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  • 1
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    IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-02
    Description: Tumor necrosis factor-alpha (TNF-alpha) is an important mediator of insulin resistance in obesity and diabetes through its ability to decrease the tyrosine kinase activity of the insulin receptor (IR). Treatment of cultured murine adipocytes with TNF-alpha was shown to induce serine phosphorylation of insulin receptor substrate 1 (IRS-1) and convert IRS-1 into an inhibitor of the IR tyrosine kinase activity in vitro. Myeloid 32D cells, which lack endogenous IRS-1, were resistant to TNF-alpha-mediated inhibition of IR signaling, whereas transfected 32D cells that express IRS-1 were very sensitive to this effect of TNF-alpha. An inhibitory form of IRS-1 was observed in muscle and fat tissues from obese rats. These results indicate that TNF-alpha induces insulin resistance through an unexpected action of IRS-1 to attenuate insulin receptor signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hotamisligil, G S -- Peraldi, P -- Budavari, A -- Ellis, R -- White, M F -- Spiegelman, B M -- DK 42539/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 2;271(5249):665-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Biology, Dana-Farber Cancer Institute, Boston, MA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8571133" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/*metabolism ; Adipose Tissue/metabolism ; Animals ; Cells, Cultured ; Insulin/pharmacology ; Insulin Receptor Substrate Proteins ; Insulin Resistance/*physiology ; Male ; Mice ; Muscle, Skeletal/metabolism ; Obesity/*metabolism ; Phosphoproteins/metabolism/*physiology ; Phosphorylation ; Rats ; Rats, Zucker ; Receptor, Insulin/*antagonists & inhibitors/metabolism ; Serine/metabolism ; Signal Transduction ; Tumor Necrosis Factor-alpha/*pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 2
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    Angiopoietin-2, a natural antagonist for Tie2 that disrupts in vivo angiogenesis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: Angiogenesis is thought to depend on a precise balance of positive and negative regulation. Angiopoietin-1 (Ang1) is an angiogenic factor that signals through the endothelial cell-specific Tie2 receptor tyrosine kinase. Like vascular endothelial growth factor, Ang1 is essential for normal vascular development in the mouse. An Ang1 relative, termed angiopoietin-2 (Ang2), was identified by homology screening and shown to be a naturally occurring antagonist for Ang1 and Tie2. Transgenic overexpression of Ang2 disrupts blood vessel formation in the mouse embryo. In adult mice and humans, Ang2 is expressed only at sites of vascular remodeling. Natural antagonists for vertebrate receptor tyrosine kinases are atypical; thus, the discovery of a negative regulator acting on Tie2 emphasizes the need for exquisite regulation of this angiogenic receptor system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maisonpierre, P C -- Suri, C -- Jones, P F -- Bartunkova, S -- Wiegand, S J -- Radziejewski, C -- Compton, D -- McClain, J -- Aldrich, T H -- Papadopoulos, N -- Daly, T J -- Davis, S -- Sato, T N -- Yancopoulos, G D -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):55-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regeneron Pharmaceuticals Inc., 777 Old Saw Mill River Road, Tarrytown, NY 10591, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204896" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Angiopoietin-1 ; Angiopoietin-2 ; Animals ; Blood Vessels/embryology/*metabolism ; Cells, Cultured ; Cloning, Molecular ; Embryo, Mammalian/metabolism ; Endothelial Growth Factors/genetics/metabolism ; Endothelium, Vascular/*cytology/metabolism ; Female ; Humans ; Ligands ; Lymphokines/genetics/metabolism ; Membrane Glycoproteins/antagonists & inhibitors/metabolism ; Mice ; Mice, Transgenic ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/chemistry/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptor Protein-Tyrosine Kinases/*antagonists & inhibitors/metabolism ; Receptor, TIE-2 ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Amidation of bioactive peptides: the structure of peptidylglycine alpha-hydroxylating monooxygenase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: Many neuropeptides and peptide hormones require amidation at the carboxyl terminus for activity. Peptidylglycine alpha-amidating monooxygenase (PAM) catalyzes the amidation of these diverse physiological regulators. The amino-terminal domain of the bifunctional PAM protein is a peptidylglycine alpha-hydroxylating monooxygenase (PHM) with two coppers that cycle through cupric and cuprous oxidation states. The anomalous signal of the endogenous coppers was used to determine the structure of the catalytic core of oxidized rat PHM with and without bound peptide substrate. These structures strongly suggest that the PHM reaction proceeds via activation of substrate by a copper-bound oxygen species. The mechanistic and structural insight gained from the PHM structures can be directly extended to dopamine beta-monooxygenase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Prigge, S T -- Kolhekar, A S -- Eipper, B A -- Mains, R E -- Amzel, L M -- DK32949/DK/NIDDK NIH HHS/ -- GM44692/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1300-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biophysical Chemistry, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360928" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Catalysis ; Copper/chemistry/metabolism ; Crystallography, X-Ray ; Dipeptides/metabolism ; Dopamine beta-Hydroxylase/chemistry/metabolism ; Electrons ; Hydroxylation ; Ligands ; Mixed Function Oxygenases/*chemistry/metabolism ; Models, Molecular ; *Multienzyme Complexes ; Oxidation-Reduction ; Oxygen/metabolism ; Peptides/metabolism ; *Protein Conformation ; Protein Structure, Secondary ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Gene discovery offers tentative clues to Parkinson's (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1973.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosome Mapping ; Chromosomes, Human, Pair 4 ; Genetic Markers ; Humans ; Lewy Bodies/chemistry ; Mice ; Mice, Transgenic ; Nerve Tissue Proteins/analysis/chemistry/*genetics ; Oxidative Stress ; Parkinson Disease/etiology/*genetics ; Point Mutation ; Protein Conformation ; Protein Folding ; Rats ; Synucleins
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    NGF signals ride a trolley to nucleus (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1037.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289850" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Axonal Transport ; Axons/*metabolism ; Cell Nucleus/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; Gene Expression Regulation ; Nerve Growth Factors/*metabolism ; Neurons/*metabolism ; Proto-Oncogene Proteins/metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/metabolism ; *Signal Transduction
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Neurogenesis in postnatal rat spinal cord: a study in primary culture (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: Spinal cord injuries result in paralysis, because when damaged neurons die they are not replaced. Neurogenesis of electrophysiologically functional neurons occurred in spinal cord cultured from postnatal rats. In these cultures, the numbers of immunocytochemically identified neurons increased over time. Additionally, neurons identified immunocytochemically or electrophysiologically incorporated bromodeoxyuridine, confirming they had differentiated from mitotic cells in vitro. These findings suggest that postnatal spinal cord retains the capacity to generate functional neurons. The presence of neuronal precursor cells in postnatal spinal cord may offer new therapeutic approaches for restoration of function to individuals with spinal cord injuries.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kehl, L J -- Fairbanks, C A -- Laughlin, T M -- Wilcox, G L -- DA07097/DA/NIDA NIH HHS/ -- DA07234/DA/NIDA NIH HHS/ -- DE00225/DE/NIDCR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):586-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate Program in Neuroscience, University of Minnesota, Minneapolis, MN 55455, USA. 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9110976" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Bromodeoxyuridine/metabolism ; Cell Differentiation ; Cells, Cultured ; Culture Media ; Glial Fibrillary Acidic Protein/analysis ; Immunohistochemistry ; Mitosis ; Neurons/chemistry/*cytology/metabolism ; Phosphopyruvate Hydratase/analysis ; Rats ; Spinal Cord/chemistry/*cytology ; Tubulin/analysis
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Rat model for Gulf War syndrome? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1404.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411763" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Disease Models, Animal ; Hippocampus/*drug effects/metabolism ; Humans ; Isoflurophate/*toxicity ; Maze Learning/drug effects ; Military Personnel ; Nicotinic Antagonists/toxicity ; Persian Gulf Syndrome/*chemically induced/metabolism ; Rats ; Receptors, Nicotinic/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Marijuana: harder than thought? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):1967-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9221496" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/metabolism ; Animals ; Brain/*drug effects/metabolism ; *Cannabis ; Corticotropin-Releasing Hormone/*metabolism ; Dopamine/*metabolism ; Dronabinol/adverse effects/*pharmacology ; Humans ; Naloxone/pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Rats ; Substance Withdrawal Syndrome/*metabolism ; Substance-Related Disorders/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 9
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    Regulatory phosphorylation of AMPA-type glutamate receptors by CaM-KII during long-term potentiation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Long-term potentiation (LTP), a cellular model of learning and memory, requires calcium-dependent protein kinases. Induction of LTP increased the phosphorus-32 labeling of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors (AMPA-Rs), which mediate rapid excitatory synaptic transmission. This AMPA-R phosphorylation appeared to be catalyzed by Ca2+- and calmodulin-dependent protein kinase II (CaM-KII): (i) it correlated with the activation and autophosphorylation of CaM-KII, (ii) it was blocked by the CaM-KII inhibitor KN-62, and (iii) its phosphorus-32 peptide map was the same as that of GluR1 coexpressed with activated CaM-KII in HEK-293 cells. This covalent modulation of AMPA-Rs in LTP provides a postsynaptic molecular mechanism for synaptic plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barria, A -- Muller, D -- Derkach, V -- Griffith, L C -- Soderling, T R -- NS27037/NS/NINDS NIH HHS/ -- R01 GM054408/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2042-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, Oregon Health Sciences University, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197267" target="_blank"〉PubMed〈/a〉
    Keywords: 1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine/analogs & derivatives/pharmacology ; 2-Amino-5-phosphonovalerate/pharmacology ; Animals ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; Cell Line ; Enzyme Inhibitors/pharmacology ; Excitatory Amino Acid Antagonists/pharmacology ; Hippocampus/*metabolism ; Humans ; In Vitro Techniques ; *Long-Term Potentiation/drug effects ; Male ; Peptide Mapping ; Phosphorylation ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Synaptic Transmission/drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Large porous particles for pulmonary drug delivery (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-20
    Description: A new type of inhalation aerosol, characterized by particles of small mass density and large size, permitted the highly efficient delivery of inhaled therapeutics into the systemic circulation. Particles with mass densities less than 0.4 gram per cubic centimeter and mean diameters exceeding 5 micrometers were inspired deep into the lungs and escaped the lungs' natural clearance mechanisms until the inhaled particles delivered their therapeutic payload. Inhalation of large porous insulin particles resulted in elevated systemic levels of insulin and suppressed systemic glucose levels for 96 hours, whereas small nonporous insulin particles had this effect for only 4 hours. High systemic bioavailability of testosterone was also achieved by inhalation delivery of porous particles with a mean diameter (20 micrometers) approximately 10 times that of conventional inhaled therapeutic particles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Edwards, D A -- Hanes, J -- Caponetti, G -- Hrkach, J -- Ben-Jebria, A -- Eskew, M L -- Mintzes, J -- Deaver, D -- Lotan, N -- Langer, R -- GM26698/GM/NIGMS NIH HHS/ -- HD29125/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 20;276(5320):1868-71.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemical Engineering, Pennsylvania State University, 204 Fenske Laboratory, University Park, PA 16802, USA. dxe11@psuv.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9188534" target="_blank"〉PubMed〈/a〉
    Keywords: *Administration, Inhalation ; Aerosols ; Animals ; Biological Availability ; Blood Glucose/analysis ; Bronchoalveolar Lavage ; *Drug Carriers ; Drug Compounding ; Insulin/administration & dosage/blood/pharmacokinetics ; *Lactic Acid ; *Lung ; Male ; Particle Size ; *Polyglycolic Acid ; *Polylysine ; *Polymers ; Rats ; Rats, Sprague-Dawley ; Testosterone/administration & dosage/blood/pharmacokinetics
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Experiments in a Parkinson's rat model (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallini, R -- Consales, A -- Lauretti, L -- Fernandez, E -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):389-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518368" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dopamine/physiology ; Fluorescent Dyes/*metabolism ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Nerve Degeneration ; Nerve Growth Factors/genetics ; Nerve Tissue Proteins/*genetics ; Neurons/metabolism/pathology ; *Neuroprotective Agents ; Oxidopamine/pharmacology ; Parkinson Disease/pathology/*therapy ; Rats ; *Stilbamidines ; Substantia Nigra/metabolism/*pathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    A neural substrate of prediction and reward (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: The capacity to predict future events permits a creature to detect, model, and manipulate the causal structure of its interactions with its environment. Behavioral experiments suggest that learning is driven by changes in the expectations about future salient events such as rewards and punishments. Physiological work has recently complemented these studies by identifying dopaminergic neurons in the primate whose fluctuating output apparently signals changes or errors in the predictions of future salient and rewarding events. Taken together, these findings can be understood through quantitative theories of adaptive optimizing control.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schultz, W -- Dayan, P -- Montague, P R -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1593-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Physiology, University of Fribourg, CH-1700 Fribourg, Switzerland. Wolfram.Schultz@unifr.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054347" target="_blank"〉PubMed〈/a〉
    Keywords: Algorithms ; Animals ; Computer Simulation ; Conditioning (Psychology) ; Cues ; Dopamine/*physiology ; *Learning ; Mesencephalon/*physiology ; *Models, Neurological ; Neurons/*physiology ; Rats ; *Reward
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Alternative cleavage of Alzheimer-associated presenilins during apoptosis by a caspase-3 family protease (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-18
    Description: Most cases of early-onset familial Alzheimer's disease (FAD) are caused by mutations in the genes encoding the presenilin 1 (PS1) and PS2 proteins, both of which undergo regulated endoproteolytic processing. During apoptosis, PS1 and PS2 were shown to be cleaved at sites distal to their normal cleavage sites by a caspase-3 family protease. In cells expressing PS2 containing the asparagine-141 FAD mutant, the ratio of alternative to normal PS2 cleavage fragments was increased relative to wild-type PS2-expressing cells, suggesting a potential role for apoptosis-associated cleavage of presenilins in the pathogenesis of Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kim, T W -- Pettingell, W H -- Jung, Y K -- Kovacs, D M -- Tanzi, R E -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):373-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Genetics and Aging Unit, Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9219695" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/*genetics/metabolism/pathology ; Amino Acid Chloromethyl Ketones/pharmacology ; Amino Acid Substitution ; Animals ; *Apoptosis ; Caspase 3 ; *Caspases ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Enzyme Activation ; Etoposide/pharmacology ; Membrane Proteins/chemistry/genetics/*metabolism ; Mutation ; Oligopeptides/pharmacology ; Phosphorylation ; Presenilin-1 ; Presenilin-2 ; Rats ; Staurosporine/pharmacology ; Tumor Cells, Cultured
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  • 14
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    NMDA channel regulation by channel-associated protein tyrosine kinase Src (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: The N-methyl-D-aspartate (NMDA) receptor mediates synaptic transmission and plasticity in the central nervous system (CNS) and is regulated by tyrosine phosphorylation. In membrane patches excised from mammalian central neurons, the endogenous tyrosine kinase Src was shown to regulate the activity of NMDA channels. The action of Src required a sequence [Src(40-58)] within the noncatalytic, unique domain of Src. In addition, Src coprecipitated with NMDA receptor proteins. Finally, endogenous Src regulated the function of NMDA receptors at synapses. Thus, NMDA receptor regulation by Src may be important in development, plasticity, and pathology in the CNS.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yu, X M -- Askalan, R -- Keil, G J 2nd -- Salter, M W -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):674-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Hospital for Sick Children, Department of Physiology, University of Toronto, Toronto, Ontario, M5G 1X8 Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005855" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Ion Channel Gating ; Ion Channels/*metabolism ; Molecular Sequence Data ; N-Methylaspartate/metabolism ; Neurons/*metabolism ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Phosphorylation ; Phosphotyrosine/metabolism ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/*metabolism ; Spinal Cord/cytology ; Synapses/*metabolism ; Synaptic Transmission ; src-Family Kinases/chemistry/*metabolism
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    Fear of hope (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Young, W -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):1907.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9333941" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Cell Transplantation ; Genetic Therapy ; Humans ; Immunotherapy ; *Nerve Regeneration ; Neuroglia/*transplantation ; Olfactory Bulb/cytology/transplantation ; Rats ; Spinal Cord Injuries/surgery/*therapy
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  • 16
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    The product of the proto-oncogene c-cbl: a negative regulator of the Syk tyrosine kinase (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-18
    Description: Engagement of antigen and immunoglobulin receptors on hematopoietic cells is directly coupled to activation of nonreceptor protein tyrosine kinases (PTKs) that then phosphorylate critical intracellular substrates. In mast cells stimulated through the FcvarepsilonRI receptor, activation of several PTKs including Syk leads to degranulation and release of such mediators of the allergic response as histamine and serotonin. Regulation of Syk function occurred through interaction with the Cbl protein, itself a PTK substrate in this system. Overexpression of Cbl led to inhibition of Syk and suppression of serotonin release from mast cells, demonstrating its ability to inhibit a nonreceptor tyrosine kinase. Complex adaptor proteins such as Cbl can directly regulate the functions of the proteins they bind.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ota, Y -- Samelson, L E -- New York, N.Y. -- Science. 1997 Apr 18;276(5311):418-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cell Biology and Metabolism Branch, National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD 20892-5430, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9103201" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Degranulation ; Enzyme Precursors/antagonists & inhibitors/*metabolism ; Genetic Vectors ; Intracellular Signaling Peptides and Proteins ; Mast Cells/*metabolism ; Mutation ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-cbl ; Rats ; Receptors, IgE/metabolism ; Receptors, IgG/metabolism ; Recombinant Proteins/metabolism ; Serotonin/metabolism ; Signal Transduction ; Tumor Cells, Cultured ; *Ubiquitin-Protein Ligases ; Vaccinia virus
    Print ISSN: 0036-8075
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  • 17
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    A synaptically controlled, associative signal for Hebbian plasticity in hippocampal neurons (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: The role of back-propagating dendritic action potentials in the induction of long-term potentiation (LTP) was investigated in CA1 neurons by means of dendritic patch recordings and simultaneous calcium imaging. Pairing of subthreshold excitatory postsynaptic potentials (EPSPs) with back-propagating action potentials resulted in an amplification of dendritic action potentials and evoked calcium influx near the site of synaptic input. This pairing also induced a robust LTP, which was reduced when EPSPs were paired with non-back-propagating action potentials or when stimuli were unpaired. Action potentials thus provide a synaptically controlled, associative signal to the dendrites for Hebbian modifications of synaptic strength.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Magee, J C -- Johnston, D -- MH44754/MH/NIMH NIH HHS/ -- NS09482/NS/NINDS NIH HHS/ -- NS11535/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):209-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA. jmagee@ptp.bcm.tmc.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985013" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Axons/physiology ; Calcium/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/drug effects/physiology ; Dendrites/*physiology ; Feedback ; In Vitro Techniques ; Long-Term Potentiation/drug effects/*physiology ; Patch-Clamp Techniques ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; *Synaptic Transmission/drug effects ; Tetrodotoxin/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 18
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    A bitter battle over insulin gene (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marshall, E -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1028-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9289846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; California ; *Cloning, Molecular ; DNA, Recombinant ; Drug Industry ; *Genetic Research ; *Genetic Vectors ; Guideline Adherence/legislation & jurisprudence ; Humans ; Insulin/*genetics ; National Institutes of Health (U.S.) ; *Patents as Topic ; *Plasmids ; Rats ; Recombinant Proteins ; Scientific Misconduct/*legislation & jurisprudence ; United States ; Universities
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Molecules give new insights into deadliest brain cancers (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1226.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411748" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brevican ; Carrier Proteins/genetics/*physiology ; Chloride Channels/*physiology ; Chondroitin Sulfate Proteoglycans ; Glioma/*metabolism/*pathology/therapy ; Humans ; Lectins, C-Type ; Neoplasm Invasiveness ; Nerve Tissue Proteins/genetics/*physiology ; Neuroglia/metabolism ; Rats ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 20
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    Seeing the synapse (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kelner, K L -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):547.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148416" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Calcium-Binding Proteins ; Cells, Cultured ; Electric Stimulation ; Hippocampus ; Membrane Glycoproteins/metabolism ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Neurons/metabolism ; Neurotransmitter Agents/*metabolism ; R-SNARE Proteins ; Rats ; Recombinant Fusion Proteins/metabolism ; Synapses/*metabolism ; Synaptic Transmission ; Synaptotagmins
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  • 21
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    The year of the dendrite (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sejnowski, T J -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):178-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute at the Salk Institute for Biological Studies, University of California, San Diego, CA 92186, USA. terry@salk.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999546" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/metabolism ; Cerebral Cortex/cytology/*physiology ; Dendrites/*physiology ; Ion Channels ; Long-Term Potentiation ; Neuronal Plasticity ; Pyramidal Cells/*physiology ; Rats ; Synapses/physiology ; Synaptic Transmission
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  • 22
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    Calcium waves in retinal glial cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-07
    Description: Calcium signals were recorded from glial cells in acutely isolated rat retina to determine whether Ca2+ waves occur in glial cells of intact central nervous system tissue. Chemical (adenosine triphosphate), electrical, and mechanical stimulation of astrocytes initiated increases in the intracellular concentration of Ca2+ that propagated at approximately 23 micrometers per second through astrocytes and Muller cells as intercellular waves. The Ca2+ waves persisted in the absence of extracellular Ca2+ but were largely abolished by thapsigargin and intracellular heparin, indicating that Ca2+ was released from intracellular stores. The waves did not evoke changes in cell membrane potential but traveled synchronously in astrocytes and Muller cells, suggesting a functional linkage between these two types of glial cells. Such glial Ca2+ waves may constitute an extraneuronal signaling pathway in the central nervous system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410141/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2410141/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Newman, E A -- Zahs, K R -- EY04077/EY/NEI NIH HHS/ -- EY10383/EY/NEI NIH HHS/ -- R01 EY004077/EY/NEI NIH HHS/ -- R01 EY004077-19/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):844-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Minnesota, 435 Delaware Street, SE, Minneapolis, MN 55455, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012354" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/pharmacology ; Animals ; Astrocytes/*metabolism ; Calcium/*metabolism ; Calcium Channels/metabolism ; Electric Stimulation ; Heparin/pharmacology ; In Vitro Techniques ; Inositol 1,4,5-Trisphosphate Receptors ; Kinetics ; Membrane Potentials ; Neuroglia/*metabolism ; Physical Stimulation ; Rats ; Receptors, Cytoplasmic and Nuclear/metabolism ; Retina/*cytology/metabolism ; Signal Transduction ; Stimulation, Chemical ; Thapsigargin/pharmacology
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  • 23
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    Nuclear export of NF-ATc enhanced by glycogen synthase kinase-3 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-28
    Description: The transcription factor NF-AT responds to Ca2+-calcineurin signals by translocating to the nucleus, where it participates in the activation of early immune response genes. Calcineurin dephosphorylates conserved serine residues in the amino terminus of NF-AT, resulting in nuclear import. Purification of the NF-AT kinase revealed that it is composed of a priming kinase activity and glycogen synthase kinase-3 (GSK-3). GSK-3 phosphorylates conserved serines necessary for nuclear export, promotes nuclear exit, and thereby opposes Ca2+-calcineurin signaling. Because GSK-3 responds to signals initiated by Wnt and other ligands, NF-AT family members could be effectors of these pathways.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beals, C R -- Sheridan, C M -- Turck, C W -- Gardner, P -- Crabtree, G R -- New York, N.Y. -- Science. 1997 Mar 28;275(5308):1930-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9072970" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Biological Transport ; Brain/enzymology ; COS Cells ; Calcineurin ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/*metabolism ; Calmodulin-Binding Proteins/metabolism ; Cell Nucleus/*metabolism ; Cloning, Molecular ; Cyclic AMP-Dependent Protein Kinases/metabolism ; DNA-Binding Proteins/genetics/*metabolism ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinases ; Humans ; Molecular Sequence Data ; NFATC Transcription Factors ; *Nuclear Proteins ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; Transcription Factors/genetics/*metabolism ; Transfection
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  • 24
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    Curing rat glioblastoma: immunotherapy or graft rejection? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-04
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beutler, A S -- Banck, M S -- Aguzzi, A -- New York, N.Y. -- Science. 1997 Apr 4;276(5309):20-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9122700" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Glioblastoma/*immunology/*therapy ; *Graft Rejection ; Histocompatibility Antigens/*immunology ; Insulin-Like Growth Factor I/*genetics ; Major Histocompatibility Complex ; Neoplasm Transplantation ; RNA, Antisense/*therapeutic use ; Rats ; Transplantation, Homologous ; Tumor Cells, Cultured
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  • 25
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    Removal of osteoclast bone resorption products by transcytosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-11
    Description: Osteoclasts are multinucleated cells responsible for bone resorption. During the resorption cycle, osteoclasts undergo dramatic changes in their polarity, and resorbing cells reveal four functionally and structurally different membrane domains. Bone degradation products, both organic and inorganic, were endocytosed from the ruffled border membrane. They were then found to be transported in vesicles through the cell to the plasma membrane domain, located in the middle of the basal membrane, where they were liberated into the extracellular space. These results explain how resorbing osteoclasts can simultaneously remove large amounts of matrix degradation products and penetrate into bone.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Salo, J -- Lehenkari, P -- Mulari, M -- Metsikko, K -- Vaananen, H K -- New York, N.Y. -- Science. 1997 Apr 11;276(5310):270-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Biocenter, University of Oulu, Kajaanintie 52 A, 90220 Oulu, Finland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9092479" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/metabolism ; Animals ; Biological Transport ; Biotin/metabolism ; Bone Matrix/*metabolism ; *Bone Resorption ; Cattle ; Cell Membrane/metabolism/ultrastructure ; Cell Polarity ; Cells, Cultured ; Endocytosis ; Extracellular Space/metabolism ; Microscopy, Confocal ; Microscopy, Electron ; Minerals/metabolism ; Organelles/metabolism ; Osteocalcin/metabolism ; Osteoclasts/*metabolism/ultrastructure ; Rats ; Tetracycline/metabolism
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  • 26
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    The importance of a well-groomed child (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R M -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1620-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, Stanford University, Stanford, CA 94305, USA. sapolsky@leland.stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9312858" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn ; *Behavior, Animal ; Corticotropin-Releasing Hormone/metabolism ; Female ; Glucocorticoids/secretion ; *Grooming ; *Handling (Psychology) ; Hippocampus/physiology ; Humans ; *Maternal Behavior ; Rats ; Receptors, Glucocorticoid/metabolism
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  • 27
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    How does the brain organize memories? (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Eichenbaum, H -- New York, N.Y. -- Science. 1997 Jul 18;277(5324):330-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Boston University, Boston, MA 02215, USA. hbe@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518364" target="_blank"〉PubMed〈/a〉
    Keywords: Amnesia/physiopathology/psychology ; Animals ; Brain Mapping ; Cerebral Cortex/*physiology ; Cues ; Haplorhini ; Hippocampus/*physiology ; Humans ; *Memory ; Neural Pathways ; Neurons/physiology ; Rats
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  • 28
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    Regulation of gliogenesis in the central nervous system by the JAK-STAT signaling pathway (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: A mechanism by which members of the ciliary neurotrophic factor (CNTF)-leukemia inhibitory factor cytokine family regulate gliogenesis in the developing mammalian central nervous system was characterized. Activation of the CNTF receptor promoted differentiation of cerebral cortical precursor cells into astrocytes and inhibited differentiation of cortical precursors along a neuronal lineage. Although CNTF stimulated both the Janus kinase-signal transducer and activator of transcription (JAK-STAT) and Ras-mitogen-activated protein kinase signaling pathways in cortical precursor cells, the JAK-STAT signaling pathway selectively enhanced differentiation of these precursors along a glial lineage. These findings suggest that cytokine activation of the JAK-STAT signaling pathway may be a mechanism by which cell fate is controlled during mammalian development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bonni, A -- Sun, Y -- Nadal-Vicens, M -- Bhatt, A -- Frank, D A -- Rozovsky, I -- Stahl, N -- Yancopoulos, G D -- Greenberg, M E -- NIHP30-HD 18655/HD/NICHD NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):477-83.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuroscience, Children's Hospital, and Department of Neurobiology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334309" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD/metabolism ; Astrocytes/*cytology/drug effects/metabolism ; Cell Differentiation ; Cell Division ; Cell Lineage ; Cells, Cultured ; Cerebral Cortex/*cytology/embryology ; Ciliary Neurotrophic Factor ; Cytokine Receptor gp130 ; DNA-Binding Proteins/*metabolism ; Dimerization ; Glial Fibrillary Acidic Protein/biosynthesis ; Growth Inhibitors/metabolism/pharmacology ; *Interleukin-6 ; Janus Kinase 1 ; Leukemia Inhibitory Factor ; Leukemia Inhibitory Factor Receptor alpha Subunit ; Lymphokines/metabolism/pharmacology ; Membrane Glycoproteins/metabolism ; Nerve Growth Factors/pharmacology ; Nerve Tissue Proteins/metabolism/pharmacology ; Platelet-Derived Growth Factor/pharmacology ; Protein-Tyrosine Kinases/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/metabolism ; Receptor, Ciliary Neurotrophic Factor ; Receptors, Cytokine/metabolism ; Receptors, Nerve Growth Factor/metabolism ; Receptors, OSM-LIF ; STAT1 Transcription Factor ; STAT3 Transcription Factor ; *Signal Transduction ; Stem Cells/cytology ; Trans-Activators/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 29
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    Postsynaptic glutamate transport at the climbing fiber-Purkinje cell synapse (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: The role of postsynaptic, neuronal glutamate transporters in terminating signals at central excitatory synapses is not known. Stimulation of a climbing fiber input to cerebellar Purkinje cells was shown to generate an anionic current mediated by glutamate transporters. The kinetics of transporter currents were resolved by pulses of glutamate to outside-out membrane patches from Purkinje cells. Comparison of synaptic transporter currents to transporter currents expressed in Xenopus oocytes suggests that postsynaptic uptake at the climbing fiber synapse removes at least 22 percent of released glutamate. These neuronal transporter currents arise from synchronous activation of transporters that greatly outnumber activated AMPA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Otis, T S -- Kavanaugh, M P -- Jahr, C E -- NS21419/NS/NINDS NIH HHS/ -- NS33270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Vollum Institute, L-474, Oregon Health Sciences University, 3181 Southwest Sam Jackson Park Road, Portland, OR 97201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278516" target="_blank"〉PubMed〈/a〉
    Keywords: *Amino Acid Transport System X-AG ; Animals ; Aspartic Acid/analogs & derivatives/pharmacology ; Biological Transport ; Carrier Proteins/*metabolism ; Dicarboxylic Acids/pharmacology ; Glutamate Plasma Membrane Transport Proteins ; Glutamic Acid/*metabolism ; In Vitro Techniques ; Kinetics ; Nerve Fibers/*metabolism ; Oocytes ; Patch-Clamp Techniques ; Purkinje Cells/*metabolism ; Pyrrolidines/pharmacology ; Rats ; Receptors, AMPA/metabolism ; Receptors, Glutamate/*metabolism ; *Symporters ; Synapses/*metabolism ; *Synaptic Transmission ; Xenopus
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    Induction of cell migration by matrix metalloprotease-2 cleavage of laminin-5 (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-11
    Description: Structural changes in the extracellular matrix are necessary for cell migration during tissue remodeling and tumor invasion. Specific cleavage of laminin-5 (Ln-5) by matrix metalloprotease-2 (MMP2) was shown to induce migration of breast epithelial cells. MMP2 cleaved the Ln-5 gamma2 subunit at residue 587, exposing a putative cryptic promigratory site on Ln-5 that triggers cell motility. This altered form of Ln-5 is found in tumors and in tissues undergoing remodeling, but not in quiescent tissues. Cleavage of Ln-5 by MMP2 and the resulting activation of the Ln-5 cryptic site may provide new targets for modulation of tumor cell invasion and tissue remodeling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Giannelli, G -- Falk-Marzillier, J -- Schiraldi, O -- Stetler-Stevenson, W G -- Quaranta, V -- CA47858/CA/NCI NIH HHS/ -- DE10063/DE/NIDCR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 11;277(5323):225-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Scripps Research Institute, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9211848" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast/*cytology/metabolism ; Cell Adhesion ; Cell Adhesion Molecules/*metabolism ; Cell Division ; Cell Line ; *Cell Movement ; Cell Size ; Collagenases/metabolism ; Epithelial Cells ; Epithelium/metabolism ; Extracellular Matrix/*metabolism ; Female ; Fibrinolysin/metabolism ; Gelatinases/antagonists & inhibitors/*metabolism ; Humans ; Matrix Metalloproteinase 2 ; Matrix Metalloproteinase 9 ; Metalloendopeptidases/antagonists & inhibitors/*metabolism ; Mice ; Phenylalanine/analogs & derivatives/pharmacology ; Protease Inhibitors/pharmacology ; Rats ; Recombinant Fusion Proteins/metabolism ; Skin Neoplasms/metabolism/pathology ; Thiophenes/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Peripheral and cerebral asymmetries in the rat (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-23
    Description: Rats learn a novel foraging pattern better with their right-side whiskers than with their left-side whiskers. They also learn better with the left cerebral hemisphere than with the right hemisphere. Rotating an already learned maze relative to the external environment most strongly reduces right-whisker performance; starting an already learned maze at a different location most strongly reduces left-whisker performance. These results suggest that the right-periphery-left-hemisphere system accesses a map-like representation of the foraging problem, whereas the left-periphery-right-hemisphere system accesses a rote path. Thus, as in humans, functional asymmetries in rats can be elicited by both peripheral and cortical manipulation, and each hemisphere makes qualitatively distinct contributions to a complex natural behavior.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LaMendola, N P -- Bever, T G -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):483-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Arizona, Tucson, AZ 85721, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334310" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; *Dominance, Cerebral ; Functional Laterality ; Male ; *Maze Learning ; Rats ; Rats, Sprague-Dawley ; Vibrissae/*physiology
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    Spatially and functionally distinct Ca2+ stores in sarcoplasmic and endoplasmic reticulum (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-03-14
    Description: The organization of calcium (Ca2+) stores in the sarcoplasmic and endoplasmic reticulum (S-ER) is poorly understood. The dynamics of the storage and release of calcium in the S-ER of intact, cultured astrocytes and arterial myocytes were studied with high-resolution imaging methods. The S-ER appeared to be a continuous tubular network; nevertheless, calcium stores in the S-ER were organized into small, spatially distinct compartments that functioned as discrete units. Cyclopiazonic acid (an inhibitor of the calcium pump in the S-ER membrane) and caffeine or ryanodine unloaded different, spatially separate compartments. Heterogeneity of calcium stores was also revealed in cells activated by physiological agonists. These results suggest that cells can generate spatially and temporally distinct calcium signals to control individual calcium-dependent processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Golovina, V A -- Blaustein, M P -- HL-32276/HL/NHLBI NIH HHS/ -- NS-16106/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Mar 14;275(5306):1643-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Center for Vascular Biology and Hypertension, University of Maryland School of Medicine, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9054358" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/*metabolism/ultrastructure ; Caffeine/pharmacology ; Calcium/*metabolism ; Calcium-Transporting ATPases/antagonists & inhibitors ; Cells, Cultured ; Endoplasmic Reticulum, Smooth/*metabolism/ultrastructure ; Fluorescent Dyes/metabolism ; Fura-2/analogs & derivatives/metabolism ; Glutamic Acid/pharmacology ; Indoles/pharmacology ; Mice ; Mitochondria/metabolism ; Mitochondria, Muscle/metabolism ; Muscle, Smooth, Vascular/cytology/*metabolism/ultrastructure ; Rats ; Ryanodine/pharmacology ; Sarcoplasmic Reticulum/*metabolism/ultrastructure ; Serotonin/pharmacology
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    Defective excitation-contraction coupling in experimental cardiac hypertrophy and heart failure (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-05-02
    Description: Cardiac hypertrophy and heart failure caused by high blood pressure were studied in single myocytes taken from hypertensive rats (Dahl SS/Jr) and SH-HF rats in heart failure. Confocal microscopy and patch-clamp methods were used to examine excitation-contraction (EC) coupling, and the relation between the plasma membrane calcium current (ICa) and evoked calcium release from the sarcoplasmic reticulum (SR), which was visualized as "calcium sparks." The ability of ICa to trigger calcium release from the SR in both hypertrophied and failing hearts was reduced. Because ICa density and SR calcium-release channels were normal, the defect appears to reside in a change in the relation between SR calcium-release channels and sarcolemmal calcium channels. beta-Adrenergic stimulation largely overcame the defect in hypertrophic but not failing heart cells. Thus, the same defect in EC coupling that develops during hypertrophy may contribute to heart failure when compensatory mechanisms fail.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gomez, A M -- Valdivia, H H -- Cheng, H -- Lederer, M R -- Santana, L F -- Cannell, M B -- McCune, S A -- Altschuld, R A -- Lederer, W J -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1997 May 2;276(5313):800-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and the Medical Biotechnology Center, University of Maryland School of Medicine, 725 West Lombard Street, Baltimore, MD 21201, USA. Universit.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9115206" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Animals ; Calcium/*metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels/metabolism ; Calcium Channels, L-Type ; Cardiomegaly/etiology/*physiopathology ; Cell Membrane/metabolism ; Heart Failure/etiology/*physiopathology ; Hypertension/complications ; Isoproterenol/pharmacology ; Microscopy, Confocal ; Muscle Proteins/metabolism ; Myocardial Contraction/drug effects/*physiology ; Myocardium/*metabolism ; Nifedipine/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Inbred Strains ; Ryanodine Receptor Calcium Release Channel ; Sarcoplasmic Reticulum/metabolism
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    Dopamine's role (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gray, J A -- Young, A M -- Joseph, M H -- New York, N.Y. -- Science. 1997 Nov 28;278(5343):1548-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology) ; Dopamine/metabolism/*physiology ; Humans ; Nucleus Accumbens/*metabolism ; Rats ; Reinforcement (Psychology)
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    Phosphorylation of the translational repressor PHAS-I by the mammalian target of rapamycin (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-04
    Description: The immunosuppressant rapamycin interferes with G1-phase progression in lymphoid and other cell types by inhibiting the function of the mammalian target of rapamycin (mTOR). mTOR was determined to be a terminal kinase in a signaling pathway that couples mitogenic stimulation to the phosphorylation of the eukaryotic initiation factor (eIF)-4E-binding protein, PHAS-I. The rapamycin-sensitive protein kinase activity of mTOR was required for phosphorylation of PHAS-I in insulin-stimulated human embryonic kidney cells. mTOR phosphorylated PHAS-I on serine and threonine residues in vitro, and these modifications inhibited the binding of PHAS-I to eIF-4E. These studies define a role for mTOR in translational control and offer further insights into the mechanism whereby rapamycin inhibits G1-phase progression in mammalian cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brunn, G J -- Hudson, C C -- Sekulic, A -- Williams, J M -- Hosoi, H -- Houghton, P J -- Lawrence, J C Jr -- Abraham, R T -- AR41189/AR/NIAMS NIH HHS/ -- DK28312/DK/NIDDK NIH HHS/ -- DK50628/DK/NIDDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):99-101.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, VA 22908, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204908" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Proteins, Signal Transducing ; Androstadienes/pharmacology ; Animals ; Carrier Proteins/pharmacology ; Cell Line ; DNA-Binding Proteins/pharmacology ; Eukaryotic Initiation Factor-4E ; G1 Phase ; Heat-Shock Proteins/pharmacology ; Humans ; Insulin/pharmacology ; Peptide Initiation Factors/metabolism ; Phosphoproteins/genetics/*metabolism ; Phosphorylation ; Phosphotransferases (Alcohol Group Acceptor)/antagonists & inhibitors/*metabolism ; Polyenes/*pharmacology ; *Protein Kinases ; Rats ; Recombinant Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; Signal Transduction ; Sirolimus ; TOR Serine-Threonine Kinases ; Tacrolimus Binding Proteins ; Transfection ; Tumor Cells, Cultured
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    Blood flow regulation by S-nitrosohemoglobin in the physiological oxygen gradient (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: The binding of oxygen to heme irons in hemoglobin promotes the binding of nitric oxide (NO) to cysteinebeta93, forming S-nitrosohemoglobin. Deoxygenation is accompanied by an allosteric transition in S-nitrosohemoglobin [from the R (oxygenated) to the T (deoxygenated) structure] that releases the NO group. S-nitrosohemoglobin contracts blood vessels and decreases cerebral perfusion in the R structure and relaxes vessels to improve blood flow in the T structure. By thus sensing the physiological oxygen gradient in tissues, hemoglobin exploits conformation-associated changes in the position of cysteinebeta93 SNO to bring local blood flow into line with oxygen requirements.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stamler, J S -- Jia, L -- Eu, J P -- McMahon, T J -- Demchenko, I T -- Bonaventura, J -- Gernert, K -- Piantadosi, C A -- HL 52529/HL/NHLBI NIH HHS/ -- HR59130/HR/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2034-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Duke University Medical Center, Room 321 MSRB, Box 2612, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197264" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Pressure ; *Cerebrovascular Circulation ; Cysteine/chemistry/metabolism ; *Hemodynamics ; Hemoglobins/analysis/chemistry/*physiology ; *Mercaptoethanol ; Models, Molecular ; Nitric Oxide/blood/metabolism ; Nitroso Compounds/blood ; Oxygen/*blood ; Oxyhemoglobins/chemistry ; Protein Conformation ; Rats ; Rats, Sprague-Dawley ; *S-Nitrosothiols
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    Proinsulin C-peptide--biological activity? (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Steiner, D F -- Rubenstein, A H -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):531-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, University of Chicago, Chicago, IL 60637, USA. dfsteine@midway.uchicago.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9254422" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/metabolism ; C-Peptide/chemistry/pharmacology/*physiology ; Capillary Permeability/drug effects ; Cell Membrane/metabolism ; Diabetes Mellitus, Experimental/drug therapy/*physiopathology ; Humans ; Insulin/chemistry/metabolism ; Models, Molecular ; Neural Conduction ; Proinsulin/chemistry ; Protein Folding ; Rats ; Sodium-Potassium-Exchanging ATPase/metabolism
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    Dual role of phosphatidylinositol-3,4,5-trisphosphate in the activation of protein kinase B (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: Protein kinase B (PKB) is a proto-oncogene that is activated in signaling pathways initiated by phosphoinositide 3-kinase. Chromatographic separation of brain cytosol revealed a kinase activity that phosphorylated and activated PKB only in the presence of phosphatidylinositol-3,4,5-trisphosphate [PtdIns(3,4,5)P3]. Phosphorylation occurred exclusively on threonine-308, a residue implicated in activation of PKB in vivo. PtdIns(3,4,5)P3 was determined to have a dual role: Its binding to the pleckstrin homology domain of PKB was required to allow phosphorylation by the upstream kinase and it directly activated the upstream kinase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokoe, D -- Stephens, L R -- Copeland, T -- Gaffney, P R -- Reese, C B -- Painter, G F -- Holmes, A B -- McCormick, F -- Hawkins, P T -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):567-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Onyx Pharmaceuticals, 3031 Research Drive, Richmond, CA 94806, USA. stokoe@cc.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228007" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Adenosine Triphosphate/metabolism ; Amino Acid Sequence ; Animals ; Blood Proteins/chemistry ; Brain/enzymology ; COS Cells ; Cytosol/enzymology ; Enzyme Activation ; Humans ; Male ; Molecular Sequence Data ; Phosphatidylinositol Phosphates/*metabolism ; *Phosphoproteins ; Phosphorylation ; Phosphothreonine/metabolism ; Protein-Serine-Threonine Kinases/chemistry/*metabolism ; Proto-Oncogene Proteins/chemistry/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Stereoisomerism
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    Sensitization to morphine induced by viral-mediated gene transfer (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: Repeated administration of morphine sensitizes animals to the stimulant and rewarding properties of the drug. It also selectively increases expression of GluR1 (an AMPA glutamate receptor subunit) in the ventral tegmental area, a midbrain region implicated in morphine action. By viral-mediated gene transfer, a causal relation is shown between these behavioral and biochemical adaptations: Morphine's stimulant and rewarding properties are intensified after microinjections of a viral vector expressing GluR1 into the ventral tegmental area. These results confirm the importance of AMPA receptors in morphine action and demonstrate specific locomotor and motivational adaptations resulting from altered expression of a single localized gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlezon, W A Jr -- Boundy, V A -- Haile, C N -- Lane, S B -- Kalb, R G -- Neve, R L -- Nestler, E J -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):812-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Yale University School of Medicine, Connecticut Mental Health Center, 34 Park Street, New Haven, CT 06508, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9242609" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/metabolism ; Conditioning, Classical ; *Gene Transfer Techniques ; Genetic Vectors ; Injections, Subcutaneous ; Male ; Morphine/administration & dosage/*pharmacology ; Motor Activity/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*genetics/*physiology ; Reward ; Simplexvirus/genetics ; Transgenes ; Tyrosine 3-Monooxygenase/metabolism ; Up-Regulation ; Ventral Tegmental Area/*drug effects/metabolism
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    Marijuana addiction (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grinspoon, L -- Bakalar, J B -- Zimmer, L -- Morgan, J P -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):749; author reply 750-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273692" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cannabis ; Dopamine/metabolism ; Dronabinol/antagonists & inhibitors/pharmacology ; Humans ; Nucleus Accumbens/drug effects/metabolism ; Rats ; Reward ; Substance Withdrawal Syndrome ; *Substance-Related Disorders
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    Repair of adult rat corticospinal tract by transplants of olfactory ensheathing cells (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-26
    Description: The upper cervical corticospinal tract was transected on one side in adult rats. A suspension of ensheathing cells cultured from adult rat olfactory bulb was injected into the lesion site. This induced unbranched, elongative growth of the cut corticospinal axons. The axons grew through the transplant and continued to regenerate into the denervated caudal host tract. Rats with complete transections and no transplanted cells did not use the forepaw on the lesioned side for directed reaching. Rats in which the transplanted cells had formed a continuous bridge across the lesion exhibited directed forepaw reaching on the lesioned side.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Y -- Field, P M -- Raisman, G -- New York, N.Y. -- Science. 1997 Sep 26;277(5334):2000-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Norman and Sadie Lee Research Centre, Division of Neurobiology, National Institute for Medical Research, Medical Research Council, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9302296" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/ultrastructure ; Brain Tissue Transplantation ; Cell Transplantation ; Cells, Cultured ; Denervation ; Female ; Microscopy, Electron ; Myelin Sheath/physiology ; *Nerve Regeneration ; Neuroglia/physiology/*transplantation/ultrastructure ; Olfactory Bulb/*cytology ; Olfactory Nerve/*cytology ; Rats ; Spinal Cord/*physiology ; Spinal Cord Injuries/*surgery
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    Measuring serotonin distribution in live cells with three-photon excitation (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-24
    Description: Tryptophan and serotonin were imaged with infrared illumination by three-photon excitation (3PE) of their native ultraviolet (UV) fluorescence. This technique, established by 3PE cross section measurements of tryptophan and the monoamines serotonin and dopamine, circumvents the limitations imposed by photodamage, scattering, and indiscriminate background encountered in other UV microscopies. Three-dimensionally resolved images are presented along with measurements of the serotonin concentration ( approximately 50 mM) and content (up to approximately 5 x 10(8) molecules) of individual secretory granules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maiti, S -- Shear, J B -- Williams, R M -- Zipfel, W R -- Webb, W W -- RR04224/RR/NCRR NIH HHS/ -- RR07719/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 24;275(5299):530-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Applied and Engineering Physics, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999797" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Cytoplasmic Granules/*chemistry ; Dopamine/analysis ; Lasers ; Microscopy, Fluorescence/instrumentation/*methods ; Photochemistry ; *Photons ; Rats ; Serotonin/*analysis ; Tryptophan/analysis ; Tumor Cells, Cultured ; Ultraviolet Rays
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    Regulation of synaptic efficacy by coincidence of postsynaptic APs and EPSPs (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Activity-driven modifications in synaptic connections between neurons in the neocortex may occur during development and learning. In dual whole-cell voltage recordings from pyramidal neurons, the coincidence of postsynaptic action potentials (APs) and unitary excitatory postsynaptic potentials (EPSPs) was found to induce changes in EPSPs. Their average amplitudes were differentially up- or down-regulated, depending on the precise timing of postsynaptic APs relative to EPSPs. These observations suggest that APs propagating back into dendrites serve to modify single active synaptic connections, depending on the pattern of electrical activity in the pre- and postsynaptic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Markram, H -- Lubke, J -- Frotscher, M -- Sakmann, B -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):213-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Max-Planck-Institut fur Medizinische Forschung, Abteilung Zellphysiologie, Jahnstrasse 29, D-69120 Heidelberg, Germany. bnmark@weizmann.weizmann.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985014" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/metabolism ; Cerebral Cortex/cytology/physiology ; Dendrites/*physiology ; Down-Regulation ; Electric Stimulation ; In Vitro Techniques ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; *Synaptic Transmission ; Time Factors ; Up-Regulation
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    An NGF-TrkA-mediated retrograde signal to transcription factor CREB in sympathetic neurons (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: Nerve growth factor (NGF) is a neurotrophic factor secreted by cells that are the targets of innervation of sympathetic and some sensory neurons. However, the mechanism by which the NGF signal is propagated from the axon terminal to the cell body, which can be more than 1 meter away, to influence biochemical events critical for growth and survival of neurons has remained unclear. An NGF-mediated signal transmitted from the terminals and distal axons of cultured rat sympathetic neurons to their nuclei regulated phosphorylation of the transcription factor CREB (cyclic adenosine monophosphate response element-binding protein). Internalization of NGF and its receptor tyrosine kinase TrkA, and their transport to the cell body, were required for transmission of this signal. The tyrosine kinase activity of TrkA was required to maintain it in an autophosphorylated state upon its arrival in the cell body and for propagation of the signal to CREB within neuronal nuclei. Thus, an NGF-TrkA complex is a messenger that delivers the NGF signal from axon terminals to cell bodies of sympathetic neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Riccio, A -- Pierchala, B A -- Ciarallo, C L -- Ginty, D D -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1097-100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Johns Hopkins University School of Medicine, 725 North Wolfe Street, Baltimore, MD 21205, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262478" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Axonal Transport ; Axons/*metabolism ; Carbazoles/pharmacology ; Cell Membrane/metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/*metabolism ; Indole Alkaloids ; Microspheres ; Nerve Growth Factors/*metabolism/pharmacology ; Neurons/*metabolism ; Phosphorylation ; Proto-Oncogene Proteins/antagonists & inhibitors/*metabolism ; Rats ; Receptor Protein-Tyrosine Kinases/antagonists & inhibitors/*metabolism ; Receptor, trkA ; Receptors, Nerve Growth Factor/antagonists & inhibitors/*metabolism ; Signal Transduction ; Superior Cervical Ganglion/cytology
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    Requirement for the CD95 receptor-ligand pathway in c-Myc-induced apoptosis (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-11-21
    Description: Induction of apoptosis by oncogenes like c-myc may be important in restraining the emergence of neoplasia. However, the mechanism by which c-myc induces apoptosis is unknown. CD95 (also termed Fas or APO-1) is a cell surface transmembrane receptor of the tumor necrosis factor receptor family that activates an intrinsic apoptotic suicide program in cells upon binding either its ligand CD95L or antibody. c-myc-induced apoptosis was shown to require interaction on the cell surface between CD95 and its ligand. c-Myc acts downstream of the CD95 receptor by sensitizing cells to the CD95 death signal. Moreover, IGF-I signaling and Bcl-2 suppress c-myc-induced apoptosis by also acting downstream of CD95. These findings link two apoptotic pathways previously thought to be independent and establish the dependency of Myc on CD95 signaling for its killing activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hueber, A O -- Zornig, M -- Lyon, D -- Suda, T -- Nagata, S -- Evan, G I -- New York, N.Y. -- Science. 1997 Nov 14;278(5341):1305-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Imperial Cancer Research Fund (ICRF) Laboratories, 44 Lincoln's Inn Fields, London WC2A 3PX, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9360929" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/*metabolism ; *Apoptosis ; Autocrine Communication ; Carrier Proteins/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cells, Cultured ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Gene Expression Regulation ; Genes, myc ; Insulin-Like Growth Factor I/pharmacology/physiology ; Membrane Glycoproteins/*metabolism ; Mice ; Proto-Oncogene Proteins c-bcl-2/pharmacology/physiology ; Proto-Oncogene Proteins c-myc/*metabolism ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Good pain, bad pain (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Iadarola, J M -- Caudle, R M -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):239-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Pain and Neurosensory Mechanisms Branch, National Institute of Dental Research, NIH, Bethesda, MD 20892-4410, USA. iadarola@yoda.nidr.nih.gov〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340772" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Gene Expression Regulation ; Humans ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Isoenzymes/genetics/*metabolism ; Mice ; Mutation ; *N-Glycosyl Hydrolases ; Neuronal Plasticity ; Neurons/*metabolism/pathology ; Pain/physiopathology ; *Pain Management ; Plant Proteins/*administration & dosage ; Protein Kinase C/genetics/*metabolism ; Rats ; Receptors, Neurokinin-1/biosynthesis ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord ; Substance P/administration & dosage
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    Maternal care, hippocampal glucocorticoid receptors, and hypothalamic-pituitary-adrenal responses to stress (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-12
    Description: Variations in maternal care affect the development of individual differences in neuroendocrine responses to stress in rats. As adults, the offspring of mothers that exhibited more licking and grooming of pups during the first 10 days of life showed reduced plasma adrenocorticotropic hormone and corticosterone responses to acute stress, increased hippocampal glucocorticoid receptor messenger RNA expression, enhanced glucocorticoid feedback sensitivity, and decreased levels of hypothalamic corticotropin-releasing hormone messenger RNA. Each measure was significantly correlated with the frequency of maternal licking and grooming (all r's 〉 -0.6). These findings suggest that maternal behavior serves to "program" hypothalamic-pituitary-adrenal responses to stress in the offspring.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Liu, D -- Diorio, J -- Tannenbaum, B -- Caldji, C -- Francis, D -- Freedman, A -- Sharma, S -- Pearson, D -- Plotsky, P M -- Meaney, M J -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1659-62.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Developmental Neuroendocrinology Laboratory, Douglas Hospital Research Center, McGill University, Montreal, Canada H4H 1R3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287218" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood ; Animals ; Animals, Newborn ; Corticosterone/blood/pharmacology ; Corticotropin-Releasing Hormone/genetics ; Feedback ; Female ; Gene Expression Regulation ; Grooming ; Handling (Psychology) ; Hippocampus/*physiology ; Hypothalamo-Hypophyseal System/*physiology ; *Maternal Behavior ; Pituitary-Adrenal System/*physiology ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Glucocorticoid/genetics/*metabolism ; Stress, Physiological/*physiopathology
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    Synaptic depression and cortical gain control (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-01-10
    Description: Cortical neurons receive synaptic inputs from thousands of afferents that fire action potentials at rates ranging from less than 1 hertz to more than 200 hertz. Both the number of afferents and their large dynamic range can mask changes in the spatial and temporal pattern of synaptic activity, limiting the ability of a cortical neuron to respond to its inputs. Modeling work based on experimental measurements indicates that short-term depression of intracortical synapses provides a dynamic gain-control mechanism that allows equal percentage rate changes on rapidly and slowly firing afferents to produce equal postsynaptic responses. Unlike inhibitory and adaptive mechanisms that reduce responsiveness to all inputs, synaptic depression is input-specific, leading to a dramatic increase in the sensitivity of a neuron to subtle changes in the firing patterns of its afferents.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abbott, L F -- Varela, J A -- Sen, K -- Nelson, S B -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):220-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Volen Center, Brandeis University, Waltham, MA 02254, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985017" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Electric Stimulation ; In Vitro Techniques ; *Models, Neurological ; Neuronal Plasticity ; Neurons/*physiology ; Neurons, Afferent/physiology ; Rats ; Synapses/*physiology ; *Synaptic Transmission ; Visual Cortex/physiology
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    Prevention of vascular and neural dysfunction in diabetic rats by C-peptide (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-07-25
    Description: C-peptide, a cleavage product from the processing of proinsulin to insulin, has been considered to possess little if any biological activity other than its participation in insulin synthesis. Injection of human C-peptide prevented or attenuated vascular and neural (electrophysiological) dysfunction and impaired Na+- and K+-dependent adenosine triphosphate activity in tissues of diabetic rats. Nonpolar amino acids in the midportion of the peptide were required for these biological effects. Synthetic reverse sequence (retro) and all-D-amino acid (enantio) C-peptides were equipotent to native C-peptide, which indicates that the effects of C-peptide on diabetic vascular and neural dysfunction were mediated by nonchiral interactions instead of stereospecific receptors or binding sites.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ido, Y -- Vindigni, A -- Chang, K -- Stramm, L -- Chance, R -- Heath, W F -- DiMarchi, R D -- Di Cera, E -- Williamson, J R -- EY 06600/EY/NEI NIH HHS/ -- HL 39934/HL/NHLBI NIH HHS/ -- HL 58141/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jul 25;277(5325):563-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9228006" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Blood Circulation/drug effects ; Blood Glucose/metabolism ; C-Peptide/*chemistry/pharmacology/*therapeutic use ; Capillary Permeability/drug effects ; Circular Dichroism ; Diabetes Mellitus, Experimental/drug therapy/physiopathology ; Diabetic Angiopathies/*prevention & control ; Diabetic Neuropathies/*prevention & control ; Humans ; Male ; Molecular Sequence Data ; Neural Conduction/drug effects ; Peptide Fragments/pharmacology ; Protein Structure, Secondary ; Rats ; Rats, Sprague-Dawley ; Sodium-Potassium-Exchanging ATPase/metabolism ; Stereoisomerism
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    Activation of corticotropin-releasing factor in the limbic system during cannabinoid withdrawal (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-27
    Description: Corticotropin-releasing factor (CRF) has been implicated in the mediation of the stress-like and negative affective consequences of withdrawal from drugs of abuse, such as alcohol, cocaine, and opiates. This study sought to determine whether brain CRF systems also have a role in cannabinoid dependence. Rats were treated daily for 2 weeks with the potent synthetic cannabinoid HU-210. Withdrawal, induced by the cannabinoid antagonist SR 141716A, was accompanied by a marked elevation in extracellular CRF concentration and a distinct pattern of Fos activation in the central nucleus of the amygdala. Maximal increases in CRF corresponded to the time when behavioral signs resulting from cannabinoid withdrawal were at a maximum. These data suggest that long-term cannabinoid administration alters CRF function in the limbic system of the brain, in a manner similar to that observed with other drugs of abuse, and also induces neuroadaptive processes that may result in future vulnerability to drug dependence.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodriguez de Fonseca, F -- Carrera, M R -- Navarro, M -- Koob, G F -- Weiss, F -- DA 08426/DA/NIDA NIH HHS/ -- DK26741/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2050-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Instituto Complutense de Drogodependencias, Departamento de Psicobiologia, Facultad de Psicologia, Universidad Complutense de Madrid, 28223 Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197270" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/*metabolism ; Animals ; Anxiety/chemically induced ; Behavior, Animal/drug effects ; Brain/drug effects/*metabolism ; Corticosterone/blood ; Corticotropin-Releasing Hormone/*metabolism ; Dronabinol/adverse effects/*analogs & derivatives/antagonists & ; inhibitors/pharmacology ; Male ; Microdialysis ; Piperidines/pharmacology ; Proto-Oncogene Proteins c-fos/analysis ; Pyrazoles/pharmacology ; Rats ; Rats, Wistar ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors ; Substance Withdrawal Syndrome/metabolism
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    Paradoxical improvement of impulse conduction in cardiac tissue by partial cellular uncoupling (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-02-07
    Description: Generally, impulse propagation in cardiac tissue is assumed to be impaired by a reduction of intercellular electrical coupling or by the presence of structural discontinuities. Contrary to this notion, the spatially uniform reduction of electrical coupling induced successful conduction in discontinuous cardiac tissue structures exhibiting unidirectional conduction block. This seemingly paradoxical finding can be explained by a nonsymmetric effect of uncoupling on the current source and the current sink in the preparations used. It suggests that partial cellular uncoupling might prevent the initiation of cardiac arrhythmias that are dependent on the presence of unidirectional conduction block.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohr, S -- Kucera, J P -- Fast, V G -- Kleber, A G -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):841-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Bern, Buhlplatz 5, CH-3012 Bern, Switzerland. rohr@pyl.unibe.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012353" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Arrhythmias, Cardiac/physiopathology ; Cells, Cultured ; Diffusion ; Fatty Acids, Monounsaturated/pharmacology ; Gap Junctions/physiology ; Heart/*physiology ; Heart Conduction System/*physiology ; Microscopy, Video ; Rats
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    Neuroscience. More than just frequency detectors? (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thomson, A M -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):179-80.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, Royal Free Hospital School of Medicine, London NW3 2PF, UK. alext@rfhsm.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8999547" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Dendrites/physiology ; Interneurons/physiology ; *Models, Neurological ; Neurotransmitter Agents/metabolism ; Probability ; Pyramidal Cells/*physiology ; Rats ; Synapses/*physiology ; *Synaptic Transmission
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    Evolution of a strain of CJD that induces BSE-like plaques (1997)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1997-07-04
    Description: Bovine spongiform encephalopathy (BSE) has become a public health issue because a recently evolved BSE agent has infected people, yielding an unusual form of Creutzfeld-Jakob disease (CJD). A new CJD agent that provokes similar amyloid plaques and cerebellar pathology was serially propagated. First-passage rats showed obvious clinical signs and activated microglia but had negligible PrP-res (the more protease-resistant form of host PrP) or cerebellar lesions. Microglia and astrocytes may participate in strain selection because the agent evolved, stabilized, and reproducibly provoked BSE-like disease in subsequent passages. Early vacuolar change involving activated microglia and astrocytes preceded significant PrP-res accumulation by more than 50 days. These studies reveal several inflammatory host reactions to an exogenous agent.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manuelidis, L -- Fritch, W -- Xi, Y G -- NS12674/NS/NINDS NIH HHS/ -- NS34569/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jul 4;277(5322):94-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neuropathology, Yale Medical School, 310 Cedar Street, New Haven, CT 06510, USA. laura.manuelidis@yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9204907" target="_blank"〉PubMed〈/a〉
    Keywords: Amyloid beta-Protein Precursor/analysis ; Animals ; Astrocytes/chemistry/*ultrastructure ; Brain/*pathology ; Brain Chemistry ; Cerebellum/chemistry/pathology ; Clusterin ; Creutzfeldt-Jakob Syndrome/metabolism/*pathology ; Cricetinae ; Cricetulus ; Encephalopathy, Bovine Spongiform/metabolism/*pathology ; Glial Fibrillary Acidic Protein/genetics/metabolism ; Glycoproteins/analysis ; Inflammation ; Macrophages/chemistry/ultrastructure ; Mice ; Mice, Inbred Strains ; Microglia/chemistry/*ultrastructure ; Microscopy, Electron ; *Molecular Chaperones ; PrPSc Proteins/*analysis/pathogenicity ; RNA/metabolism ; Rats ; Rats, Sprague-Dawley ; Time Factors ; Ubiquitins/analysis ; Vacuoles/ultrastructure ; Virulence
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    Interactions between epithelial cells and bacteria, normal and pathogenic (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Umesaki, Y -- Okada, Y -- Imaoka, A -- Setoyama, H -- Matsumoto, S -- New York, N.Y. -- Science. 1997 May 9;276(5314):964-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9139662" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteroides/physiology ; Enzyme Induction ; Fucosyltransferases/biosynthesis/metabolism ; G(M1) Ganglioside/biosynthesis ; Germ-Free Life ; Gram-Positive Bacteria/*physiology ; Histocompatibility Antigens Class II/biosynthesis ; Intestinal Mucosa/cytology/immunology/metabolism/*microbiology ; Intestine, Small/cytology/immunology/metabolism/*microbiology ; Lymphocytes/cytology ; Mice ; Rats
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    Inhibition of hyperalgesia by ablation of lamina I spinal neurons expressing the substance P receptor (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-10
    Description: Substance P is released in the spinal cord in response to painful stimuli, but its role in nociceptive signaling remains unclear. When a conjugate of substance P and the ribosome-inactivating protein saporin was infused into the spinal cord, it was internalized and cytotoxic to lamina I spinal cord neurons that express the substance P receptor. This treatment left responses to mild noxious stimuli unchanged, but markedly attenuated responses to highly noxious stimuli and mechanical and thermal hyperalgesia. Thus, lamina I spinal cord neurons that express the substance P receptor play a pivotal role in the transmission of highly noxious stimuli and the maintenance of hyperalgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mantyh, P W -- Rogers, S D -- Honore, P -- Allen, B J -- Ghilardi, J R -- Li, J -- Daughters, R S -- Lappi, D A -- Wiley, R G -- Simone, D A -- MH56368/MH/NIMH NIH HHS/ -- NS23970/NS/NINDS NIH HHS/ -- NS31223/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Neurobiology Laboratory (151), Veterans Administration Medical Center, Minneapolis, MN 55417, USA. manty001@maroon.tc.umn.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9323204" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Capsaicin ; Cell Membrane/metabolism ; Cells, Cultured ; Fluorescent Antibody Technique ; Hyperalgesia/physiopathology/*therapy ; *Immunotoxins ; Injections, Spinal ; *N-Glycosyl Hydrolases ; Neurons/cytology/*metabolism ; Pain/physiopathology ; *Pain Management ; Pain Measurement ; Plant Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Neurokinin-1/biosynthesis/*metabolism ; Ribosome Inactivating Proteins, Type 1 ; Signal Transduction ; Spinal Cord/*cytology/metabolism ; Substance P/*metabolism/pharmacology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Cancer chemopreventive activity of resveratrol, a natural product derived from grapes (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-10
    Description: Resveratrol, a phytoalexin found in grapes and other food products, was purified and shown to have cancer chemopreventive activity in assays representing three major stages of carcinogenesis. Resveratrol was found to act as an antioxidant and antimutagen and to induce phase II drug-metabolizing enzymes (anti-initiation activity); it mediated anti-inflammatory effects and inhibited cyclooxygenase and hydroperoxidase functions (antipromotion activity); and it induced human promyelocytic leukemia cell differentiation (antiprogression activity). In addition, it inhibited the development of preneoplastic lesions in carcinogen-treated mouse mammary glands in culture and inhibited tumorigenesis in a mouse skin cancer model. These data suggest that resveratrol, a common constituent of the human diet, merits investigation as a potential cancer chemopreventive agent in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jang, M -- Cai, L -- Udeani, G O -- Slowing, K V -- Thomas, C F -- Beecher, C W -- Fong, H H -- Farnsworth, N R -- Kinghorn, A D -- Mehta, R G -- Moon, R C -- Pezzuto, J M -- P01 CA48112/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1997 Jan 10;275(5297):218-20.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicinal Chemistry and Pharmacognosy, College of Pharmacy, University of Illinois at Chicago, Chicago, IL 60612, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8985016" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Inflammatory Agents, Non-Steroidal/pharmacology/therapeutic use ; Anticarcinogenic Agents/*pharmacology/therapeutic use ; Antimutagenic Agents/pharmacology ; Carcinogens ; Cell Differentiation/drug effects ; Cyclooxygenase 1 ; Cyclooxygenase Inhibitors/pharmacology/therapeutic use ; Female ; Fruit/*chemistry ; Humans ; Inflammation/drug therapy ; Isoenzymes/metabolism ; Mammary Neoplasms, Experimental/chemically induced/prevention & control ; Membrane Proteins ; Mice ; Neoplasms, Experimental/*prevention & control ; Peroxidases/antagonists & inhibitors ; Precancerous Conditions/prevention & control ; Prostaglandin-Endoperoxide Synthases/metabolism ; Rats ; Rats, Wistar ; Skin Neoplasms/chemically induced/prevention & control ; Stilbenes/*pharmacology/therapeutic use ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Interdomain interactions underlying activation of cyclic nucleotide-gated channels (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-10-06
    Description: Cyclic nucleotide-gated (CNG) ion channels are multimeric proteins that activate in response to the binding of cyclic nucleotide to intracellular domains. Here, an intramolecular protein-protein interaction between the amino-terminal domain and the carboxyl-terminal ligand-binding domain of the rat olfactory CNG channel was shown to exert an autoexcitatory effect on channel activation. Calcium-calmodulin, which modulates CNG channel activity during odorant adaptation, blocked this interaction. A specific deletion within the amino-terminal domain disrupted the interdomain interaction in vitro and altered the gating properties and calmodulin sensitivity of expressed channels. Thus, the amino-terminal domain may promote channel opening by directly interacting with the carboxyl-terminal gating machinery; calmodulin regulates channel activity by targeting this interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Varnum, M D -- Zagotta, W N -- EY 10329/EY/NEI NIH HHS/ -- R01 EY010329/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1997 Oct 3;278(5335):110-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Biophysics, and Howard Hughes Medical Institute, Box 357370, University of Washington School of Medicine, Seattle, WA 98195, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9311913" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Calmodulin/pharmacology ; Cyclic AMP/metabolism ; Cyclic GMP/metabolism ; Cyclic Nucleotide-Gated Cation Channels ; *Ion Channel Gating ; Ion Channels/*metabolism ; Ligands ; Olfactory Receptor Neurons/*metabolism ; Patch-Clamp Techniques ; Rats ; Recombinant Fusion Proteins/metabolism ; Retinal Rod Photoreceptor Cells/metabolism ; Xenopus
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Elementary calcium-release units induced by inositol trisphosphate (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-06-13
    Description: The extent to which inositol 1,4,5-trisphosphate (InsP3)-induced calcium signals are localized is a critical parameter for understanding the mechanism of effector activation. The spatial characteristics of InsP3-mediated calcium signals were determined by targeting a dextran-based calcium indicator to intracellular membranes through the in situ addition of a geranylgeranyl lipid group. Elementary calcium-release events observed with this indicator typically lasted less than 33 milliseconds, had diameters less than 2 micrometers, and were uncoupled from each other by the calcium buffer EGTA. Cellwide calcium transients are likely to result from synchronized triggering of such local release events, suggesting that calcium-dependent effector proteins could be selectively activated by localization near sites of local calcium release.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horne, J H -- Meyer, T -- GM-51457/GM/NIGMS NIH HHS/ -- P01-HL-47053/HL/NHLBI NIH HHS/ -- R01-GM-48113/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Jun 13;276(5319):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9180077" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Cytosol/metabolism ; Egtazic Acid/pharmacology ; Electroporation ; Fluorescent Dyes ; Inositol 1,4,5-Trisphosphate/*pharmacology ; Intracellular Membranes/*metabolism ; Kinetics ; Microscopy, Confocal ; Microscopy, Fluorescence ; Organic Chemicals ; Peptides/metabolism ; Rats ; Signal Transduction ; Tumor Cells, Cultured
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Requirement of NF-kappaB activation to suppress p53-independent apoptosis induced by oncogenic Ras (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997
    Description: The ras proto-oncogene is frequently mutated in human tumors and functions to chronically stimulate signal transduction cascades resulting in the synthesis or activation of specific transcription factors, including Ets, c-Myc, c-Jun, and nuclear factor kappa B (NF-kappaB). These Ras-responsive transcription factors are required for transformation, but the mechanisms by which these proteins facilitate oncogenesis have not been fully established. Oncogenic Ras was shown to initiate a p53-independent apoptotic response that was suppressed through the activation of NF-kappaB. These results provide an explanation for the requirement of NF-kappaB for Ras-mediated oncogenesis and provide evidence that Ras-transformed cells are susceptible to apoptosis even if they do not express the p53 tumor-suppressor gene product.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mayo, M W -- Wang, C Y -- Cogswell, P C -- Rogers-Graham, K S -- Lowe, S W -- Der, C J -- Baldwin, A S Jr -- CA13106/CA/NCI NIH HHS/ -- CA52072/CA/NCI NIH HHS/ -- CA72771/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Dec 5;278(5344):1812-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lineberger Comprehensive Cancer Center, University of North Carolina School of Medicine, Chapel Hill, NC 27599, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9388187" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Adenovirus E1A Proteins/genetics/metabolism ; Animals ; *Apoptosis ; Cell Line, Transformed ; Cell Survival ; *Cell Transformation, Neoplastic ; *Gene Expression Regulation, Neoplastic ; *Genes, p53 ; *Genes, ras ; Mice ; NF-kappa B/*metabolism ; Rats ; Transfection ; Tumor Suppressor Protein p53/physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Putative cancer gene shows up in development instead (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-04-25
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roush, W -- New York, N.Y. -- Science. 1997 Apr 25;276(5312):534-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9148413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Caenorhabditis elegans/genetics/growth & development ; Cell Adhesion Molecules/*metabolism ; Central Nervous System/abnormalities/embryology/*growth & development ; Chromosomes, Human, Pair 18 ; Colorectal Neoplasms/genetics ; *Genes, DCC ; Humans ; Mice ; Nerve Growth Factors/*metabolism ; Rats ; Receptors, Cell Surface/*metabolism ; Signal Transduction ; *Tumor Suppressor Proteins
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    Marijuana addiction (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉McGregor, I S -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):749-50; author reply 750-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273693" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety ; *Cannabis ; Dopamine/*metabolism ; Dronabinol/*pharmacology ; Humans ; Nucleus Accumbens/*drug effects/metabolism ; Rats ; Reward ; *Substance-Related Disorders
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    Heat shock protein linked to stroke protection (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-12-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1997 Nov 21;278(5342):1405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9411765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Survival ; Cerebrovascular Disorders/pathology/*prevention & control/therapy ; Corpus Striatum/pathology ; Gene Transfer Techniques ; *Genetic Therapy ; Genetic Vectors ; HSP72 Heat-Shock Proteins ; Heat-Shock Proteins/*genetics/metabolism ; Neurons/metabolism/pathology ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Regulation of neuronal survival by the serine-threonine protein kinase Akt (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-01-31
    Description: A signaling pathway was delineated by which insulin-like growth factor 1 (IGF-1) promotes the survival of cerebellar neurons. IGF-1 activation of phosphoinositide 3-kinase (PI3-K) triggered the activation of two protein kinases, the serine-threonine kinase Akt and the p70 ribosomal protein S6 kinase (p70(S6K)). Experiments with pharmacological inhibitors, as well as expression of wild-type and dominant-inhibitory forms of Akt, demonstrated that Akt but not p70(S6K) mediates PI3-K-dependent survival. These findings suggest that in the developing nervous system, Akt is a critical mediator of growth factor-induced neuronal survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dudek, H -- Datta, S R -- Franke, T F -- Birnbaum, M J -- Yao, R -- Cooper, G M -- Segal, R A -- Kaplan, D R -- Greenberg, M E -- DK39519/DK/NIDDK NIH HHS/ -- R01 CA18689/CA/NCI NIH HHS/ -- R01 CA43855/CA/NCI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1997 Jan 31;275(5300):661-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology, Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9005851" target="_blank"〉PubMed〈/a〉
    Keywords: Androstadienes/pharmacology ; Animals ; *Apoptosis/drug effects ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Cell Survival/drug effects ; Cells, Cultured ; Cerebellum/cytology ; Chromones/pharmacology ; Enzyme Activation ; Enzyme Inhibitors/pharmacology ; Insulin/pharmacology ; Insulin-Like Growth Factor I/*pharmacology ; Morpholines/pharmacology ; Neurons/*cytology/drug effects/enzymology ; Phosphatidylinositol 3-Kinases ; Phosphotransferases (Alcohol Group Acceptor)/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Ribosomal Protein S6 Kinases ; *Signal Transduction ; Transfection
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    Functional role of high-affinity anandamide transport, as revealed by selective inhibition (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-08-22
    Description: Anandamide, an endogenous ligand for central cannabinoid receptors, is released from neurons on depolarization and rapidly inactivated. Anandamide inactivation is not completely understood, but it may occur by transport into cells or by enzymatic hydrolysis. The compound N-(4-hydroxyphenyl)arachidonylamide (AM404) was shown to inhibit high-affinity anandamide accumulation in rat neurons and astrocytes in vitro, an indication that this accumulation resulted from carrier-mediated transport. Although AM404 did not activate cannabinoid receptors or inhibit anandamide hydrolysis, it enhanced receptor-mediated anandamide responses in vitro and in vivo. The data indicate that carrier-mediated transport may be essential for termination of the biological effects of anandamide, and may represent a potential drug target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beltramo, M -- Stella, N -- Calignano, A -- Lin, S Y -- Makriyannis, A -- Piomelli, D -- New York, N.Y. -- Science. 1997 Aug 22;277(5329):1094-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉The Neurosciences Institute, 10640 J. J. Hopkins Drive, San Diego, CA 92121, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9262477" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics/pharmacology ; Animals ; Arachidonic Acids/antagonists & inhibitors/*metabolism/pharmacology ; Astrocytes/drug effects/*metabolism ; Benzoxazines ; Biological Transport/drug effects ; Bromcresol Green/pharmacology ; Cannabinoids/antagonists & inhibitors/*metabolism/pharmacology ; Cells, Cultured ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Endocannabinoids ; Male ; Mice ; Morpholines/pharmacology ; Naphthalenes/pharmacology ; Neurons/drug effects/*metabolism ; Piperidines/pharmacology ; Polyunsaturated Alkamides ; Pyrazoles/pharmacology ; Rats ; Receptors, Cannabinoid ; Receptors, Drug/agonists/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Differential ligand activation of estrogen receptors ERalpha and ERbeta at AP1 sites (1997)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1997-09-05
    Description: The transactivation properties of the two estrogen receptors, ERalpha and ERbeta, were examined with different ligands in the context of an estrogen response element and an AP1 element. ERalpha and ERbeta were shown to signal in opposite ways when complexed with the natural hormone estradiol from an AP1 site: with ERalpha, 17beta-estradiol activated transcription, whereas with ERbeta, 17beta-estradiol inhibited transcription. Moreover, the antiestrogens tamoxifen, raloxifene, and Imperial Chemical Industries 164384 were potent transcriptional activators with ERbeta at an AP1 site. Thus, the two ERs signal in different ways depending on ligand and response element. This suggests that ERalpha and ERbeta may play different roles in gene regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Paech, K -- Webb, P -- Kuiper, G G -- Nilsson, S -- Gustafsson, J -- Kushner, P J -- Scanlan, T S -- GM 50672/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1997 Sep 5;277(5331):1508-10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmaceutical Chemistry, University of California, San Francisco, CA 94143-0446, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9278514" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Breast Neoplasms/metabolism ; Cell Line ; Diethylstilbestrol/metabolism/pharmacology ; *Enhancer Elements, Genetic ; Estradiol/analogs & derivatives/metabolism/pharmacology ; Estrogen Antagonists/*pharmacology ; Estrogen Receptor alpha ; Estrogen Receptor beta ; Estrogens/*pharmacology ; Female ; HeLa Cells ; Humans ; Ligands ; Piperidines/metabolism/pharmacology ; Polyunsaturated Alkamides ; Raloxifene Hydrochloride ; Rats ; Receptors, Estrogen/*metabolism ; Tamoxifen/metabolism/pharmacology ; Transcription Factor AP-1/*genetics ; *Transcriptional Activation/drug effects ; Transfection ; Tumor Cells, Cultured ; Uterus/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A selective inhibitor of eIF2alpha dephosphorylation protects cells from ER stress (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-02-12
    Description: Most protein phosphatases have little intrinsic substrate specificity, making selective pharmacological inhibition of specific dephosphorylation reactions a challenging problem. In a screen for small molecules that protect cells from endoplasmic reticulum (ER) stress, we identified salubrinal, a selective inhibitor of cellular complexes that dephosphorylate eukaryotic translation initiation factor 2 subunit alpha (eIF2alpha). Salubrinal also blocks eIF2alpha dephosphorylation mediated by a herpes simplex virus protein and inhibits viral replication. These results suggest that selective chemical inhibitors of eIF2alpha dephosphorylation may be useful in diseases involving ER stress or viral infection. More broadly, salubrinal demonstrates the feasibility of selective pharmacological targeting of cellular dephosphorylation events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyce, Michael -- Bryant, Kevin F -- Jousse, Celine -- Long, Kai -- Harding, Heather P -- Scheuner, Donalyn -- Kaufman, Randal J -- Ma, Dawei -- Coen, Donald M -- Ron, David -- Yuan, Junying -- AI19838/AI/NIAID NIH HHS/ -- AI26077/AI/NIAID NIH HHS/ -- DDK42394/DK/NIDDK NIH HHS/ -- DK47119/DK/NIDDK NIH HHS/ -- ES08681/ES/NIEHS NIH HHS/ -- GM64703/GM/NIGMS NIH HHS/ -- NS35138/NS/NINDS NIH HHS/ -- R37-AG012859/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Feb 11;307(5711):935-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15705855" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Differentiation ; Apoptosis/*drug effects ; Cell Cycle Proteins ; Cell Line ; Cinnamates/*pharmacology/toxicity ; *Cytoprotection ; Dose-Response Relationship, Drug ; Endoplasmic Reticulum/*metabolism ; Enzyme Inhibitors/pharmacology ; Eukaryotic Initiation Factor-2/*metabolism ; Genes, Reporter ; Herpesvirus 1, Human/drug effects/physiology ; Keratitis, Herpetic/drug therapy/virology ; Male ; Mice ; Oxazoles/pharmacology/toxicity ; PC12 Cells ; Phosphoprotein Phosphatases/metabolism ; Phosphorylation ; Protein Folding ; Protein Kinases/metabolism ; Protein Phosphatase 1 ; Proteins/metabolism ; Rats ; Thiourea/*analogs & derivatives/*pharmacology/toxicity ; Tunicamycin/pharmacology ; Viral Proteins/metabolism ; Virus Replication/drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    DISC1 and PDE4B are interacting genetic factors in schizophrenia that regulate cAMP signaling (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-19
    Description: The disrupted in schizophrenia 1 (DISC1) gene is a candidate susceptibility factor for schizophrenia, but its mechanistic role in the disorder is unknown. Here we report that the gene encoding phosphodiesterase 4B (PDE4B) is disrupted by a balanced translocation in a subject diagnosed with schizophrenia and a relative with chronic psychiatric illness. The PDEs inactivate adenosine 3',5'-monophosphate (cAMP), a second messenger implicated in learning, memory, and mood. We show that DISC1 interacts with the UCR2 domain of PDE4B and that elevation of cellular cAMP leads to dissociation of PDE4B from DISC1 and an increase in PDE4B activity. We propose a mechanistic model whereby DISC1 sequesters PDE4B in resting cells and releases it in an activated state in response to elevated cAMP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Millar, J Kirsty -- Pickard, Benjamin S -- Mackie, Shaun -- James, Rachel -- Christie, Sheila -- Buchanan, Sebastienne R -- Malloy, M Pat -- Chubb, Jennifer E -- Huston, Elaine -- Baillie, George S -- Thomson, Pippa A -- Hill, Elaine V -- Brandon, Nicholas J -- Rain, Jean-Christophe -- Camargo, L Miguel -- Whiting, Paul J -- Houslay, Miles D -- Blackwood, Douglas H R -- Muir, Walter J -- Porteous, David J -- G8604010/Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2005 Nov 18;310(5751):1187-91.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Genetics Section, Molecular Medicine Centre, University of Edinburgh, Edinburgh EH4 2XU, UK. Kirsty.Millar@ed.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293762" target="_blank"〉PubMed〈/a〉
    Keywords: 3',5'-Cyclic-AMP Phosphodiesterases/*genetics/metabolism ; Adult ; Affective Disorders, Psychotic/genetics/metabolism ; Animals ; Cadherins/genetics ; Cell Line ; Chromosomes, Human, Pair 1 ; Chromosomes, Human, Pair 16 ; Cyclic AMP/*metabolism ; Cyclic Nucleotide Phosphodiesterases, Type 4 ; Enzyme Activation ; Genetic Predisposition to Disease ; Humans ; Male ; Nerve Tissue Proteins/*genetics/metabolism ; Protein Binding ; Rats ; Schizophrenia/enzymology/*genetics/metabolism ; *Signal Transduction ; Translocation, Genetic
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    Long-term modulation of electrical synapses in the mammalian thalamus (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-12-17
    Description: Electrical synapses are common between inhibitory neurons in the mammalian thalamus and neocortex. Synaptic modulation, which allows flexibility of communication between neurons, has been studied extensively at chemical synapses, but modulation of electrical synapses in the mammalian brain has barely been examined. We found that the activation of metabotropic glutamate receptors, via endogenous neurotransmitter or by agonist, causes long-term reduction of electrical synapse strength between the inhibitory neurons of the rat thalamic reticular nucleus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Landisman, Carole E -- Connors, Barry W -- NS050434/NS/NINDS NIH HHS/ -- NS25983/NS/NINDS NIH HHS/ -- NS40528/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1809-13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA. Carole_Landisman@hms.harvard.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16357260" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cycloleucine/analogs & derivatives/pharmacology ; Electric Conductivity ; Electric Stimulation ; Excitatory Postsynaptic Potentials ; Gap Junctions/*physiology ; Glycine/analogs & derivatives/pharmacology ; In Vitro Techniques ; Intralaminar Thalamic Nuclei/cytology/*physiology ; Membrane Potentials ; Neocortex/physiology ; Neurons/*physiology ; Neurotransmitter Agents/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/*physiology ; Synapses/physiology
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    PERIOD1-associated proteins modulate the negative limb of the mammalian circadian oscillator (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-30
    Description: The clock proteins PERIOD1 (PER1) and PERIOD2 (PER2) play essential roles in a negative transcriptional feedback loop that generates circadian rhythms in mammalian cells. We identified two PER1-associated factors, NONO and WDR5, that modulate PER activity. The reduction of NONO expression by RNA interference (RNAi) attenuated circadian rhythms in mammalian cells, and fruit flies carrying a hypomorphic allele were nearly arrhythmic. WDR5, a subunit of histone methyltransferase complexes, augmented PER-mediated transcriptional repression, and its reduction by RNAi diminished circadian histone methylations at the promoter of a clock gene.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brown, Steven A -- Ripperger, Juergen -- Kadener, Sebastian -- Fleury-Olela, Fabienne -- Vilbois, Francis -- Rosbash, Michael -- Schibler, Ueli -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):693-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology and National Centres of Competence in Research (NCCR) Frontiers in Genetics, Sciences III, University of Geneva, 30 Quai Ernest Ansermet, CH-1211 Geneva-4, Switzerland. steven.brown@molbio.unige.ch〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15860628" target="_blank"〉PubMed〈/a〉
    Keywords: 3T3 Cells ; Animals ; Carrier Proteins/genetics/*metabolism ; Cell Cycle Proteins ; Cell Line ; *Circadian Rhythm ; DNA-Binding Proteins/genetics/metabolism ; Drosophila/genetics/physiology ; Drosophila Proteins/genetics/physiology ; Female ; Gene Expression Regulation ; Histones/metabolism ; Immunoprecipitation ; Male ; Methylation ; Mice ; Mice, Inbred BALB C ; Nuclear Proteins/genetics/*metabolism/physiology ; Nuclear Receptor Subfamily 1, Group D, Member 1 ; Period Circadian Proteins ; Promoter Regions, Genetic ; Proteins/genetics/*metabolism ; RNA Interference ; Rats ; Receptors, Cytoplasmic and Nuclear/genetics/metabolism ; Transcription Factors ; Transcription, Genetic ; Transfection
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    Self-propagating, molecular-level polymorphism in Alzheimer's beta-amyloid fibrils (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-18
    Description: Amyloid fibrils commonly exhibit multiple distinct morphologies in electron microscope and atomic force microscope images, often within a single image field. By using electron microscopy and solid-state nuclear magnetic resonance measurements on fibrils formed by the 40-residue beta-amyloid peptide of Alzheimer's disease (Abeta(1-40)), we show that different fibril morphologies have different underlying molecular structures, that the predominant structure can be controlled by subtle variations in fibril growth conditions, and that both morphology and molecular structure are self-propagating when fibrils grow from preformed seeds. Different Abeta(1-40) fibril morphologies also have significantly different toxicities in neuronal cell cultures. These results have implications for the mechanism of amyloid formation, the phenomenon of strains in prion diseases, the role of amyloid fibrils in amyloid diseases, and the development of amyloid-based nano-materials.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petkova, Aneta T -- Leapman, Richard D -- Guo, Zhihong -- Yau, Wai-Ming -- Mattson, Mark P -- Tycko, Robert -- New York, N.Y. -- Science. 2005 Jan 14;307(5707):262-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Chemical Physics, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health (NIH), Bethesda, MD 20892-0520, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15653506" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs ; Amyloid beta-Peptides/*chemistry/toxicity/*ultrastructure ; Animals ; Cells, Cultured ; Chemistry, Physical ; Hippocampus/cytology ; Humans ; Hydrogen Bonding ; Microscopy, Atomic Force ; Microscopy, Electron, Transmission ; Molecular Structure ; Neurons/cytology/drug effects ; Nuclear Magnetic Resonance, Biomolecular ; Peptide Fragments/*chemistry/toxicity/*ultrastructure ; Physicochemical Phenomena ; Protein Conformation ; Protein Structure, Secondary ; Rats
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    Neuroscience. Similar is different in hippocampal networks (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buzsaki, Gyorgy -- New York, N.Y. -- Science. 2005 Jul 22;309(5734):568-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Molecular and Behavioral Neuroscience, Rutgers University, Newark, NJ 07102, USA. buzsaki@axon.rutgers.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16040697" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cues ; Electrophysiology ; Hippocampus/cytology/*physiology ; Interneurons/physiology ; Memory/*physiology ; Nerve Net/*physiology ; Neural Inhibition ; Neurons/*physiology ; Orientation/*physiology ; Perception/physiology ; Pyramidal Cells/*physiology ; Rats ; Space Perception/*physiology
    Print ISSN: 0036-8075
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    Neuroscience. Attractors in memory (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Poucet, Bruno -- Save, Etienne -- New York, N.Y. -- Science. 2005 May 6;308(5723):799-800.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neurobiology and Cognition, CNRS-Universite Aix-Marseille, Centre Saint-Charles, 13331 Marseille Cedex 3, France. bpoucet@up.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15879197" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Brain Mapping ; Cues ; Environment ; Form Perception ; Hippocampus/*cytology/*physiology ; Learning ; Memory/*physiology ; Orientation ; Pattern Recognition, Visual ; Pyramidal Cells/*physiology ; Rats ; Space Perception
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    How visual stimuli activate dopaminergic neurons at short latency (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-03-05
    Description: Unexpected, biologically salient stimuli elicit a short-latency, phasic response in midbrain dopaminergic (DA) neurons. Although this signal is important for reinforcement learning, the information it conveys to forebrain target structures remains uncertain. One way to decode the phasic DA signal would be to determine the perceptual properties of sensory inputs to DA neurons. After local disinhibition of the superior colliculus in anesthetized rats, DA neurons became visually responsive, whereas disinhibition of the visual cortex was ineffective. As the primary source of visual afferents, the limited processing capacities of the colliculus may constrain the visual information content of phasic DA responses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dommett, Eleanor -- Coizet, Veronique -- Blaha, Charles D -- Martindale, John -- Lefebvre, Veronique -- Walton, Natalie -- Mayhew, John E W -- Overton, Paul G -- Redgrave, Peter -- New York, N.Y. -- Science. 2005 Mar 4;307(5714):1476-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, University of Sheffield, Sheffield, S10 2TP, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15746431" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicuculline/pharmacology ; Dopamine/*metabolism ; Electrochemistry ; Evoked Potentials, Visual ; Habituation, Psychophysiologic ; Neostriatum/physiology ; Neural Inhibition ; Neurons/*physiology ; *Photic Stimulation ; Rats ; *Reaction Time ; Reinforcement (Psychology) ; Reward ; Substantia Nigra/*physiology ; Superior Colliculi/*physiology ; Ventral Tegmental Area/*physiology ; Visual Cortex/physiology ; Visual Pathways/physiology
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    Uncharged tRNA and sensing of amino acid deficiency in mammalian piriform cortex (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: Recognizing a deficiency of indispensable amino acids (IAAs) for protein synthesis is vital for dietary selection in metazoans, including humans. Cells in the brain's anterior piriform cortex (APC) are sensitive to IAA deficiency, signaling diet rejection and foraging for complementary IAA sources, but the mechanism is unknown. Here we report that the mechanism for recognizing IAA-deficient foods follows the conserved general control (GC) system, wherein uncharged transfer RNA induces phosphorylation of eukaryotic initiation factor 2 (eIF2) via the GC nonderepressing 2 (GCN2) kinase. Thus, a basic mechanism of nutritional stress management functions in mammalian brain to guide food selection for survival.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hao, Shuzhen -- Sharp, James W -- Ross-Inta, Catherine M -- McDaniel, Brent J -- Anthony, Tracy G -- Wek, Ronald C -- Cavener, Douglas R -- McGrath, Barbara C -- Rudell, John B -- Koehnle, Thomas J -- Gietzen, Dorothy W -- GM49164/GM/NIGMS NIH HHS/ -- NS043231/NS/NINDS NIH HHS/ -- NS33347/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 Mar 18;307(5716):1776-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉School of Veterinary Medicine, Department of Anatomy, Physiology and Cell Biology, University of California, Davis, CA 95616, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774759" target="_blank"〉PubMed〈/a〉
    Keywords: Acylation ; Amino Acids, Essential/*administration & dosage/analysis/*deficiency ; Animals ; Diet ; Eating ; Eukaryotic Initiation Factor-2/*metabolism ; *Food ; Food Preferences ; Leucine/administration & dosage/*analogs & derivatives/pharmacology ; Mice ; Mice, Inbred C57BL ; Olfactory Pathways/*metabolism ; Phosphorylation ; Protein Kinases/*metabolism ; Protein-Serine-Threonine Kinases ; RNA, Transfer/*metabolism ; Rats ; Stereoisomerism ; Threonine/administration & dosage ; eIF-2 Kinase/metabolism
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    Environmental health. Debate continues over safety of water spiked with rocket fuel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stokstad, Erik -- New York, N.Y. -- Science. 2005 Jan 28;307(5709):507.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681361" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/drug effects/embryology ; Female ; Humans ; Maximum Allowable Concentration ; National Academy of Sciences (U.S.) ; Perchlorates/administration & dosage/*toxicity ; Pregnancy ; Rats ; Risk Assessment ; Thyroid Gland/drug effects ; Thyroid Hormones/metabolism ; Toxicity Tests ; United States ; United States Environmental Protection Agency ; Water Pollutants, Chemical/administration & dosage/*toxicity ; *Water Supply
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    Merits of a new drug trial for ALS? (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-05-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beghi, Ettore -- Bendotti, Caterina -- Mennini, Tiziana -- New York, N.Y. -- Science. 2005 Apr 29;308(5722):632-3; author reply 632-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15864832" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Transport System X-AG/biosynthesis ; Amyotrophic Lateral Sclerosis/*drug therapy ; Animals ; Anti-Bacterial Agents/pharmacology/*therapeutic use ; Biological Transport/drug effects ; Ceftriaxone/pharmacology/*therapeutic use ; Clinical Trials as Topic ; Glutamic Acid/metabolism ; Humans ; Rats ; Spinal Cord/drug effects/metabolism
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    Glial membranes at the node of Ranvier prevent neurite outgrowth (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-11-19
    Description: Nodes of Ranvier are regularly placed, nonmyelinated axon segments along myelinated nerves. Here we show that nodal membranes isolated from the central nervous system (CNS) of mammals restricted neurite outgrowth of cultured neurons. Proteomic analysis of these membranes revealed several inhibitors of neurite outgrowth, including the oligodendrocyte myelin glycoprotein (OMgp). In rat spinal cord, OMgp was not localized to compact myelin, as previously thought, but to oligodendroglia-like cells, whose processes converge to form a ring that completely encircles the nodes. In OMgp-null mice, CNS nodes were abnormally wide and collateral sprouting was observed. Nodal ensheathment in the CNS may stabilize the node and prevent axonal sprouting.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Jeffrey K -- Phillips, Greg R -- Roth, Alejandro D -- Pedraza, Liliana -- Shan, Weisong -- Belkaid, Wiam -- Mi, Sha -- Fex-Svenningsen, Asa -- Florens, Laurence -- Yates, John R 3rd -- Colman, David R -- NS20147/NS/NINDS NIH HHS/ -- P41 RR11823/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1813-7. Epub 2005 Nov 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Fishberg Department of Neuroscience, Mount Sinai School of Medicine, One Gustave L. Levy Place, New York, NY 10029, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16293723" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/analysis ; Axons/*physiology/ultrastructure ; Cattle ; Cell Surface Extensions/chemistry/*physiology/ultrastructure ; Cells, Cultured ; GPI-Linked Proteins ; Ganglia, Spinal/physiology/ultrastructure ; Humans ; Mice ; Myelin Proteins ; Myelin Sheath/chemistry ; Myelin-Associated Glycoprotein/analysis ; Myelin-Oligodendrocyte Glycoprotein ; Neurites/*physiology/ultrastructure ; Neuroglia/chemistry/*physiology/*ultrastructure ; Oligodendroglia/chemistry/physiology/ultrastructure ; Proteoglycans/analysis ; Proteomics ; Ranvier's Nodes/chemistry/*physiology/ultrastructure ; Rats ; Spinal Cord/cytology
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    Postsynaptic receptor trafficking underlying a form of associative learning (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-03-05
    Description: To elucidate molecular, cellular, and circuit changes that occur in the brain during learning, we investigated the role of a glutamate receptor subtype in fear conditioning. In this form of learning, animals associate two stimuli, such as a tone and a shock. Here we report that fear conditioning drives AMPA-type glutamate receptors into the synapse of a large fraction of postsynaptic neurons in the lateral amygdala, a brain structure essential for this learning process. Furthermore, memory was reduced if AMPA receptor synaptic incorporation was blocked in as few as 10 to 20% of lateral amygdala neurons. Thus, the encoding of memories in the lateral amygdala is mediated by AMPA receptor trafficking, is widely distributed, and displays little redundancy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rumpel, Simon -- LeDoux, Joseph -- Zador, Anthony -- Malinow, Roberto -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):83-8. Epub 2005 Mar 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cold Spring Harbor Laboratory, Cold Spring Harbor, NY 11724, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15746389" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/metabolism/*physiology/virology ; Animals ; Association Learning/*physiology ; Conditioning (Psychology) ; Electrophysiology ; Fear ; Female ; Genetic Vectors ; Green Fluorescent Proteins/metabolism ; Long-Term Potentiation ; Male ; Memory/*physiology ; Neural Pathways/physiology ; *Neuronal Plasticity ; Neurons/metabolism/*physiology/virology ; Patch-Clamp Techniques ; Protein Transport ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/*metabolism ; Recombinant Fusion Proteins/metabolism ; Simplexvirus/genetics ; Synapses/metabolism/*physiology ; Synaptic Transmission ; Thalamus/physiology
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    Vasopressin and oxytocin excite distinct neuronal populations in the central amygdala (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-04-12
    Description: Vasopressin and oxytocin strongly modulate autonomic fear responses, through mechanisms that are still unclear. We describe how these neuropeptides excite distinct neuronal populations in the central amygdala, which provides the major output of the amygdaloid complex to the autonomic nervous system. We identified these two neuronal populations as part of an inhibitory network, through which vasopressin and oxytocin modulate the integration of excitatory information from the basolateral amygdala and cerebral cortex in opposite manners. Through this network, the expression and endogenous activation of vasopressin and oxytocin receptors may regulate the autonomic expression of fear.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huber, Daniel -- Veinante, Pierre -- Stoop, Ron -- New York, N.Y. -- Science. 2005 Apr 8;308(5719):245-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular Biology and Morphology, Centre Hospitalier Universitaire Vaudois, University of Lausanne, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15821089" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/cytology/drug effects/*physiology ; Animals ; Antidiuretic Hormone Receptor Antagonists ; Autoradiography ; Fear/physiology ; In Vitro Techniques ; Neurons/*physiology ; Oxytocin/*analogs & derivatives/pharmacology/*physiology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Oxytocin/agonists/antagonists & inhibitors/metabolism ; Receptors, Vasopressin/agonists/metabolism ; Tetrodotoxin/pharmacology ; Vasopressins/*physiology ; gamma-Aminobutyric Acid/metabolism
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    Distinct kinetic changes in neurotransmitter release after SNARE protein cleavage (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-16
    Description: Neurotransmitter release is triggered by calcium ions and depends critically on the correct function of three types of SNARE [soluble N-ethylmaleimide-sensitive factor attachment protein (SNAP) receptor] proteins. With use of the large calyx of Held presynaptic terminal from rats, we found that cleavage of different SNARE proteins by clostridial neurotoxins caused distinct kinetic changes in neurotransmitter release. When elevating calcium ion concentration directly at the presynaptic terminal with the use of caged calcium, cleavage of SNAP-25 by botulinum toxin A (BoNT/A) produced a strong reduction in the calcium sensitivity for release, whereas cleavage of syntaxin using BoNT/C1 and synaptobrevin using tetanus toxin (TeNT) produced an all-or-nothing block without changing the kinetics of remaining vesicles. When stimulating release by calcium influx through channels, a difference between BoNT/C1 and TeNT emerged, which suggests that cleavage of synaptobrevin modifies the coupling between channels and release-competent vesicles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sakaba, Takeshi -- Stein, Alexander -- Jahn, Reinhard -- Neher, Erwin -- New York, N.Y. -- Science. 2005 Jul 15;309(5733):491-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Department of Membrane Biophysics, Max Planck Institute for Biophysical Chemistry, Gottingen 37077, Germany. tsakaba@gwdg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16020741" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Botulinum Toxins/metabolism/pharmacology ; Botulinum Toxins, Type A/metabolism/pharmacology ; Calcium/metabolism ; Calcium Channels/metabolism ; Excitatory Postsynaptic Potentials ; In Vitro Techniques ; Kinetics ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Presynaptic Terminals/*metabolism ; Qa-SNARE Proteins ; R-SNARE Proteins ; Rats ; Synaptic Vesicles/metabolism ; Synaptosomal-Associated Protein 25 ; Tetanus Toxin/metabolism/pharmacology
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    Neuroscience. Making synapses: a balancing act (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hussain, Natasha K -- Sheng, Morgan -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1207-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Picower Center for Learning and Memory, RIKEN-MIT Neuroscience Research Center, Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. natashah@mit.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15731430" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Adhesion Molecules, Neuronal ; Cells, Cultured ; Glutamic Acid/metabolism ; Hippocampus/cytology ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Binding ; Rats ; Synapses/*physiology ; Synaptic Membranes/*physiology ; gamma-Aminobutyric Acid/metabolism
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  • 82
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    Neuroscience. Matching at the synapse (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-05-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thompson, Scott M -- New York, N.Y. -- Science. 2005 May 6;308(5723):800-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, University of Maryland School of Medicine, Baltimore, MD 21201-1559, USA. sthom003@umaryland.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15879198" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/*metabolism ; Calcium Channels/metabolism ; Calcium Signaling ; Cell Communication ; Exocytosis ; Interneurons/*physiology ; Neuronal Plasticity ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Probability ; Pyramidal Cells/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/physiology ; Somatosensory Cortex/cytology/*physiology ; Synapses/*physiology ; Synaptic Vesicles/physiology ; gamma-Aminobutyric Acid/metabolism
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    Medicine. Low-power mitochondria may raise risk of cardiovascular problems (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-01-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marx, Jean -- New York, N.Y. -- Science. 2005 Jan 21;307(5708):334-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15661980" target="_blank"〉PubMed〈/a〉
    Keywords: Aerobiosis ; Animals ; Breeding ; Cardiovascular Diseases/*etiology/physiopathology ; Disease Models, Animal ; Exercise ; *Exercise Tolerance ; Humans ; Hypertension/physiopathology ; Insulin Resistance ; Metabolic Syndrome X/physiopathology ; Mitochondria, Muscle/metabolism/*physiology ; Obesity/etiology ; *Physical Exertion ; Rats ; Risk Factors
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  • 84
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    Psychology. Beyond a joke: from animal laughter to human joy? (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-04-02
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Panksepp, Jaak -- New York, N.Y. -- Science. 2005 Apr 1;308(5718):62-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉J. P. Scott Center for Neuroscience, Mind and Behavior, Department of Psychology, Bowling Green State University, Bowling Green, OH 43403,USA. jpankse@bgnet.bgsu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15802592" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Evolution ; Brain/physiology ; Emotions ; *Happiness ; Humans ; *Laughter ; Play and Playthings ; Rats ; *Vocalization, Animal
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  • 85
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    Identification and functional characterization of brainstem cannabinoid CB2 receptors (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-10-15
    Description: The presence and function of CB2 receptors in central nervous system (CNS) neurons are controversial. We report the expression of CB2 receptor messenger RNA and protein localization on brainstem neurons. These functional CB2 receptors in the brainstem were activated by a CB2 receptor agonist, 2-arachidonoylglycerol, and by elevated endogenous levels of endocannabinoids, which also act at CB1 receptors. CB2 receptors represent an alternative site of action of endocannabinoids that opens the possibility of nonpsychotropic therapeutic interventions using enhanced endocannabinoid levels in localized brain areas.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Van Sickle, Marja D -- Duncan, Marnie -- Kingsley, Philip J -- Mouihate, Abdeslam -- Urbani, Paolo -- Mackie, Ken -- Stella, Nephi -- Makriyannis, Alexandros -- Piomelli, Daniele -- Davison, Joseph S -- Marnett, Lawrence J -- Di Marzo, Vincenzo -- Pittman, Quentin J -- Patel, Kamala D -- Sharkey, Keith A -- GM15431/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2005 Oct 14;310(5746):329-32.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Infection, Immunity, and Inflammation and Hotchkiss Brain Institute, Department of Physiology and Biophysics, University of Calgary, Calgary, AB, Canada T2N 4N1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16224028" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arachidonic Acids/pharmacology ; Blotting, Western ; Brain Stem/*metabolism ; Cannabinoid Receptor Modulators/metabolism ; Cannabinoids/pharmacology ; Cerebellum/metabolism ; Cerebral Cortex/metabolism ; Endocannabinoids ; Ferrets ; Immunohistochemistry ; Mice ; Polyunsaturated Alkamides ; RNA, Messenger/analysis ; Rats ; Receptor, Cannabinoid, CB2/agonists/antagonists & inhibitors/*metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Vomiting/prevention & control
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    Neuroscience. Genes that guide brain development linked to dyslexia (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):759.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272090" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*growth & development/physiology ; Chromosomes, Human, Pair 6/genetics ; Dyslexia/*genetics ; Gene Expression ; Humans ; Nerve Tissue Proteins/genetics/physiology ; Neural Pathways/physiology ; *Polymorphism, Single Nucleotide ; Rats ; Reading ; Receptors, Immunologic/genetics/physiology
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    Bone marrow stromal cells generate muscle cells and repair muscle degeneration (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: Bone marrow stromal cells (MSCs) have great potential as therapeutic agents. We report a method for inducing skeletal muscle lineage cells from human and rat general adherent MSCs with an efficiency of 89%. Induced cells differentiated into muscle fibers upon transplantation into degenerated muscles of rats and mdx-nude mice. The induced population contained Pax7-positive cells that contributed to subsequent regeneration of muscle upon repetitive damage without additional transplantation of cells. These MSCs represent a more ready supply of myogenic cells than do the rare myogenic stem cells normally found in muscle and bone marrow.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dezawa, Mari -- Ishikawa, Hiroto -- Itokazu, Yutaka -- Yoshihara, Tomoyuki -- Hoshino, Mikio -- Takeda, Shin-ichi -- Ide, Chizuka -- Nabeshima, Yo-ichi -- New York, N.Y. -- Science. 2005 Jul 8;309(5732):314-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Neurobiology, Kyoto University Graduate School of Medicine, Yoshidakonoecho, Sakyo-ku, Kyoto, 606-8501 Japan. dezawa@anat2.med.kyoto-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002622" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bone Marrow Cells/*cytology/physiology ; Bone Marrow Transplantation ; *Cell Differentiation ; Cell Fusion ; Cell Lineage ; Cell Proliferation ; Cell Separation ; Cells, Cultured ; Colforsin/pharmacology ; Fibroblast Growth Factor 2/pharmacology ; Gene Expression Profiling ; Homeodomain Proteins/analysis ; Humans ; Mice ; Mice, Inbred mdx ; Mice, Nude ; Muscle Cells/*cytology ; Muscle Development/genetics ; Muscle Fibers, Skeletal/*cytology ; Muscle Proteins/analysis ; Muscle, Skeletal/cytology ; Muscular Diseases/*therapy ; Muscular Dystrophy, Duchenne/therapy ; Neuregulins/pharmacology ; PAX7 Transcription Factor ; Platelet-Derived Growth Factor/pharmacology ; Rats ; Regeneration ; Satellite Cells, Skeletal Muscle/cytology/physiology ; Stem Cells/cytology/physiology ; Stromal Cells/*cytology/physiology/transplantation ; Transfection
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    Independent codes for spatial and episodic memory in hippocampal neuronal ensembles (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-26
    Description: Hippocampal neurons were recorded under conditions in which the recording chamber was varied but its location remained unchanged versus conditions in which an identical chamber was encountered in different places. Two forms of neuronal pattern separation occurred. In the variable cue-constant place condition, the firing rates of active cells varied, often over more than an order of magnitude, whereas the location of firing remained constant. In the variable place-constant cue condition, both location and rates changed, so that population vectors for a given location in the chamber were statistically independent. These independent encoding schemes may enable simultaneous representation of spatial and episodic memory information.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Leutgeb, Stefan -- Leutgeb, Jill K -- Barnes, Carol A -- Moser, Edvard I -- McNaughton, Bruce L -- Moser, May-Britt -- New York, N.Y. -- Science. 2005 Jul 22;309(5734):619-23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre for the Biology of Memory, Medical-Technical Research Centre, Norwegian University of Science and Technology, 7489 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16040709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cues ; Electrodes, Implanted ; Electrophysiology ; Hippocampus/cytology/*physiology ; Interneurons/physiology ; Male ; Memory/*physiology ; Nerve Net/*physiology ; Neurons/*physiology ; Orientation/*physiology ; Perception/physiology ; Pyramidal Cells/*physiology ; Rats ; Rats, Long-Evans ; Space Perception/*physiology
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    Epigenetic transgenerational actions of endocrine disruptors and male fertility (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-06-04
    Description: Transgenerational effects of environmental toxins require either a chromosomal or epigenetic alteration in the germ line. Transient exposure of a gestating female rat during the period of gonadal sex determination to the endocrine disruptors vinclozolin (an antiandrogenic compound) or methoxychlor (an estrogenic compound) induced an adult phenotype in the F1 generation of decreased spermatogenic capacity (cell number and viability) and increased incidence of male infertility. These effects were transferred through the male germ line to nearly all males of all subsequent generations examined (that is, F1 to F4). The effects on reproduction correlate with altered DNA methylation patterns in the germ line. The ability of an environmental factor (for example, endocrine disruptor) to reprogram the germ line and to promote a transgenerational disease state has significant implications for evolutionary biology and disease etiology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Anway, Matthew D -- Cupp, Andrea S -- Uzumcu, Mehmet -- Skinner, Michael K -- New York, N.Y. -- Science. 2005 Jun 3;308(5727):1466-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Reproductive Biology, School of Molecular Biosciences, Washington State University, Pullman, WA 99164-4231, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15933200" target="_blank"〉PubMed〈/a〉
    Keywords: Androgen Antagonists/*toxicity ; Animals ; Crosses, Genetic ; DNA Methylation ; Endocrine Glands/*drug effects ; Environmental Pollutants/toxicity ; Epigenesis, Genetic/drug effects ; Estrogens/*toxicity ; Female ; Fertility/*drug effects/genetics ; Fungicides, Industrial/*toxicity ; Infertility, Male/chemically induced/genetics ; Inheritance Patterns ; Insecticides/*toxicity ; Male ; Methoxychlor/*toxicity ; Oxazoles/*toxicity ; Pregnancy ; Rats ; Spermatozoa/drug effects
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    Dependence of olfactory bulb neurogenesis on prokineticin 2 signaling (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-06-25
    Description: Neurogenesis persists in the olfactory bulb (OB) of the adult mammalian brain. New interneurons are continually added to the OB from the subventricular zone (SVZ) via the rostral migratory stream (RMS). Here we show that secreted prokineticin 2 (PK2) functions as a chemoattractant for SVZ-derived neuronal progenitors. Within the OB, PK2 may also act as a detachment signal for chain-migrating progenitors arriving from the RMS. PK2 deficiency in mice leads to a marked reduction in OB size, loss of normal OB architecture, and the accumulation of neuronal progenitors in the RMS. These findings define an essential role for G protein-coupled PK2 signaling in postnatal and adult OB neurogenesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ng, Kwan L -- Li, Jia-Da -- Cheng, Michelle Y -- Leslie, Frances M -- Lee, Alex G -- Zhou, Qun-Yong -- New York, N.Y. -- Science. 2005 Jun 24;308(5730):1923-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, University of California-Irvine (UCI), Irvine, CA 92697, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15976302" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apoptosis ; Brain/cytology/growth & development/metabolism ; Cell Adhesion ; Cell Count ; Cell Line ; Cell Proliferation ; Cerebral Ventricles/cytology/*physiology ; Chemotactic Factors/physiology ; Chemotaxis ; Coculture Techniques ; Dopamine/physiology ; Gastrointestinal Hormones/*metabolism ; Gene Expression ; Interneurons/cytology/*physiology ; Mice ; Mice, Inbred C57BL ; Neurons/cytology/*physiology ; Neuropeptides/*metabolism ; Olfactory Bulb/*cytology/growth & development/*metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/genetics/metabolism ; *Signal Transduction ; Stem Cells/*physiology
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    Crystal structure of a mammalian voltage-dependent Shaker family K+ channel (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-07-09
    Description: Voltage-dependent potassium ion (K+) channels (Kv channels) conduct K+ ions across the cell membrane in response to changes in the membrane voltage, thereby regulating neuronal excitability by modulating the shape and frequency of action potentials. Here we report the crystal structure, at a resolution of 2.9 angstroms, of a mammalian Kv channel, Kv1.2, which is a member of the Shaker K+ channel family. This structure is in complex with an oxido-reductase beta subunit of the kind that can regulate mammalian Kv channels in their native cell environment. The activation gate of the pore is open. Large side portals communicate between the pore and the cytoplasm. Electrostatic properties of the side portals and positions of the T1 domain and beta subunit are consistent with electrophysiological studies of inactivation gating and with the possibility of K+ channel regulation by the beta subunit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, Stephen B -- Campbell, Ernest B -- Mackinnon, Roderick -- GM43949/GM/NIGMS NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):897-903. Epub 2005 Jul 7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Laboratory of Molecular Neurobiology and Biophysics, Rockefeller University, 1230 York Avenue, New York, NY 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16002581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Catalytic Domain ; Cloning, Molecular ; Crystallography, X-Ray ; Electrochemistry ; Kv1.2 Potassium Channel ; Models, Molecular ; Pichia ; Potassium/chemistry ; Potassium Channels, Voltage-Gated/*chemistry ; Protein Conformation ; Protein Structure, Tertiary ; Protein Subunits/chemistry ; Rats ; Recombinant Proteins/chemistry
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    Control of excitatory and inhibitory synapse formation by neuroligins (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-01
    Description: The normal function of neural networks depends on a delicate balance between excitatory and inhibitory synaptic inputs. Synapse formation is thought to be regulated by bidirectional signaling between pre- and postsynaptic cells. We demonstrate that members of the Neuroligin family promote postsynaptic differentiation in cultured rat hippocampal neurons. Down-regulation of neuroligin isoform expression by RNA interference results in a loss of excitatory and inhibitory synapses. Electrophysiological analysis revealed a predominant reduction of inhibitory synaptic function. Thus, neuroligins control the formation and functional balance of excitatory and inhibitory synapses in hippocampal neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chih, Ben -- Engelman, Holly -- Scheiffele, Peter -- New York, N.Y. -- Science. 2005 Feb 25;307(5713):1324-8. Epub 2005 Jan 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology and Cellular Biophysics, Center for Neurobiology and Behavior, Columbia University, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15681343" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cell Adhesion Molecules, Neuronal ; Cell Line ; Cells, Cultured ; Dendrites/physiology/ultrastructure ; Down-Regulation ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; Hippocampus/cytology ; Membrane Proteins/genetics/*metabolism ; Membrane Transport Proteins/metabolism ; Mutation ; Nerve Tissue Proteins/genetics/*metabolism ; Neural Inhibition ; Neurons/physiology ; Presynaptic Terminals/*physiology ; Protein Isoforms ; RNA Interference ; Rats ; Receptors, AMPA/metabolism ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/*physiology ; Synaptic Membranes/*physiology ; Synaptic Transmission ; Transfection ; Vesicular Glutamate Transport Protein 1 ; Vesicular Inhibitory Amino Acid Transport Proteins
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    Biomedicine. Separation of conjoined hormones yields appetite rivals (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nogueiras, Ruben -- Tschop, Matthias -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):985-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284170" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Appetite/drug effects ; Computational Biology ; *Eating/drug effects ; Energy Metabolism ; Fasting ; Gastric Emptying/drug effects ; Gastrointestinal Motility/drug effects ; Ghrelin ; Humans ; Mice ; Peptide Hormones/genetics/metabolism/pharmacology/*physiology ; Protein Precursors/metabolism ; Protein Processing, Post-Translational ; Rats ; Receptors, G-Protein-Coupled/genetics/metabolism ; Signal Transduction ; Stomach/metabolism ; Weight Gain/drug effects
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  • 94
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    Obestatin, a peptide encoded by the ghrelin gene, opposes ghrelin's effects on food intake (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-15
    Description: Ghrelin, a circulating appetite-inducing hormone, is derived from a prohormone by posttranslational processing. On the basis of the bioinformatic prediction that another peptide also derived from proghrelin exists, we isolated a hormone from rat stomach and named it obestatin-a contraction of obese, from the Latin "obedere," meaning to devour, and "statin," denoting suppression. Contrary to the appetite-stimulating effects of ghrelin, treatment of rats with obestatin suppressed food intake, inhibited jejunal contraction, and decreased body-weight gain. Obestatin bound to the orphan G protein-coupled receptor GPR39. Thus, two peptide hormones with opposing action in weight regulation are derived from the same ghrelin gene. After differential modification, these hormones activate distinct receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhang, Jian V -- Ren, Pei-Gen -- Avsian-Kretchmer, Orna -- Luo, Ching-Wei -- Rauch, Rami -- Klein, Cynthia -- Hsueh, Aaron J W -- New York, N.Y. -- Science. 2005 Nov 11;310(5750):996-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Reproductive Biology, Department of Obstetrics and Gynecology, Stanford University School of Medicine, Stanford, CA 94305-5317, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16284174" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; CHO Cells ; Computational Biology ; Conserved Sequence ; Cricetinae ; *Eating/drug effects ; Fasting ; Gastric Emptying/drug effects ; Gastrointestinal Motility/drug effects ; Ghrelin ; Humans ; In Vitro Techniques ; Ligands ; Male ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Peptide Hormones/blood/chemistry/*genetics/metabolism/pharmacology/*physiology ; Protein Binding ; Protein Precursors/*genetics ; Radioimmunoassay ; Rats ; Rats, Sprague-Dawley ; Receptors, G-Protein-Coupled/metabolism ; Receptors, Ghrelin ; Signal Transduction ; Weight Gain/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 95
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    Golgin tethers define subpopulations of COPI vesicles (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-02-19
    Description: Coiled-coil proteins of the golgin family have been implicated in intra-Golgi transport through tethering coat protein complex I (COPI) vesicles. The p115-golgin tether is the best studied, and here we characterize the golgin-84-CASP tether. The vesicles bound by this tether were strikingly different from those bound by the p115-golgin tether in that they lacked members of the p24 family of putative cargo receptors and contained enzymes instead of anterograde cargo. Microinjected golgin-84 or CASP also inhibited Golgi-enzyme transport to the endoplasmic reticulum, further implicating this tether in retrograde transport. These and other golgins may modulate the flow patterns within the Golgi stack.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malsam, Jorg -- Satoh, Ayano -- Pelletier, Laurence -- Warren, Graham -- New York, N.Y. -- Science. 2005 Feb 18;307(5712):1095-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, Ludwig Institute for Cancer Research, Yale University School of Medicine, 333 Cedar Street, New Haven, CT 06520-8002, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15718469" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoantigens/*metabolism ; Binding, Competitive ; COP-Coated Vesicles/*metabolism ; Cell Fractionation ; Cell Line ; Cytoskeletal Proteins/*metabolism ; DNA-Binding Proteins ; Endoplasmic Reticulum/metabolism ; Golgi Apparatus/chemistry/enzymology/*metabolism ; Humans ; Immunoprecipitation ; Membrane Glycoproteins/metabolism ; Membrane Proteins/*metabolism ; Microscopy, Electron ; Protein Transport ; Rats ; Recombinant Fusion Proteins/metabolism ; Transcription Factors ; Viral Envelope Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
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    The widespread impact of mammalian MicroRNAs on mRNA repression and evolution (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-11-26
    Description: Thousands of mammalian messenger RNAs are under selective pressure to maintain 7-nucleotide sites matching microRNAs (miRNAs). We found that these conserved targets are often highly expressed at developmental stages before miRNA expression and that their levels tend to fall as the miRNA that targets them begins to accumulate. Nonconserved sites, which outnumber the conserved sites 10 to 1, also mediate repression. As a consequence, genes preferentially expressed at the same time and place as a miRNA have evolved to selectively avoid sites matching the miRNA. This phenomenon of selective avoidance extends to thousands of genes and enables spatial and temporal specificities of miRNAs to be revealed by finding tissues and developmental stages in which messages with corresponding sites are expressed at lower levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Farh, Kyle Kai-How -- Grimson, Andrew -- Jan, Calvin -- Lewis, Benjamin P -- Johnston, Wendy K -- Lim, Lee P -- Burge, Christopher B -- Bartel, David P -- New York, N.Y. -- Science. 2005 Dec 16;310(5755):1817-21. Epub 2005 Nov 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research, Department of Biology, Massachusetts Institute of Technology, and Howard Hughes Medical Institute, 9 Cambridge Center, Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16308420" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Base Sequence ; Cell Differentiation ; Conserved Sequence ; *Evolution, Molecular ; Gene Expression Profiling ; *Gene Expression Regulation ; Humans ; Mammals/*genetics ; Mice ; MicroRNAs/*metabolism ; Molecular Sequence Data ; Muscle Fibers, Skeletal/cytology/metabolism ; Organ Specificity ; RNA Stability ; RNA, Messenger/*genetics/metabolism ; Rats ; Species Specificity ; Untranslated Regions ; Zebrafish/genetics
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Canada. Animal rules keep grad students out of the lab (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-12-03
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kondro, Wayne -- New York, N.Y. -- Science. 2005 Dec 2;310(5753):1405.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16322427" target="_blank"〉PubMed〈/a〉
    Keywords: Animal Welfare/*legislation & jurisprudence ; Animals ; Biomedical Research/legislation & jurisprudence ; Canada ; Laboratories ; Rats ; Schools, Medical/legislation & jurisprudence ; *Students ; Universities/*legislation & jurisprudence
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
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    Target cell-dependent normalization of transmitter release at neocortical synapses (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-03-19
    Description: The efficacy and short-term modification of neocortical synaptic connections vary with the type of target neuron. We investigated presynaptic Ca2+ and release probability at single synaptic contacts between pairs of neurons in layer 2/3 of the rat neocortex. The amplitude of Ca2+ signals in boutons of pyramids contacting bitufted or multipolar interneurons or other pyramids was dependent on the target cell type. Optical quantal analysis at single synaptic contacts suggested that release probabilities are also target cell-specific. Both the Ca2+ signal and the release probability of different boutons of a pyramid contacting the same target cell varied little. We propose that the mechanisms that regulate the functional properties of boutons of a pyramid normalize the presynaptic Ca2+ influx and release probability for all those boutons that innervate the same target cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Koester, Helmut J -- Johnston, Daniel -- MH44754/MH/NIMH NIH HHS/ -- MH48432/MH/NIMH NIH HHS/ -- NNS37444/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2005 May 6;308(5723):863-6. Epub 2005 Mar 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Abteilung Zellphysiologie, Max-Planck-Institut fur Medizinische Forschung, Jahnstrasse 29, D-69120 Heidelberg, Germany. HKoester@mail.utexas.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15774725" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/physiology ; Calcium/*metabolism ; Calcium Signaling ; Dendrites/physiology ; Excitatory Postsynaptic Potentials ; Fluorescence ; In Vitro Techniques ; Interneurons/*physiology ; Models, Neurological ; Neuronal Plasticity ; Neurotransmitter Agents/*metabolism ; Patch-Clamp Techniques ; Presynaptic Terminals/physiology ; Probability ; Pyramidal Cells/*physiology ; Rats ; Rats, Wistar ; Somatosensory Cortex/cytology/*physiology ; Synapses/*physiology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
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    Neuronal activity regulates diffusion across the neck of dendritic spines (2005)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2005-11-08
    Description: In mammalian excitatory neurons, dendritic spines are separated from dendrites by thin necks. Diffusion across the neck limits the chemical and electrical isolation of each spine. We found that spine/dendrite diffusional coupling is heterogeneous and uncovered a class of diffusionally isolated spines. The barrier to diffusion posed by the neck and the number of diffusionally isolated spines is bidirectionally regulated by neuronal activity. Furthermore, coincident synaptic activation and postsynaptic action potentials rapidly restrict diffusion across the neck. The regulation of diffusional coupling provides a possible mechanism for determining the amplitude of postsynaptic potentials and the accumulation of plasticity-inducing molecules within the spine head.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bloodgood, Brenda L -- Sabatini, Bernardo L -- New York, N.Y. -- Science. 2005 Nov 4;310(5749):866-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16272125" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Cytoplasm/physiology ; Dendrites/*physiology ; Dendritic Spines/*physiology ; Diffusion ; Excitatory Postsynaptic Potentials ; Fluorescence ; GABA-A Receptor Antagonists ; Glutamic Acid/metabolism ; Green Fluorescent Proteins/metabolism ; Hippocampus/physiology ; Neurons/*physiology ; Organ Culture Techniques ; Patch-Clamp Techniques ; Pyramidal Cells/physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/antagonists & inhibitors/metabolism ; Receptors, GABA-A/metabolism ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/metabolism ; Synapses/*physiology ; Synaptic Transmission ; Transfection ; Viscosity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
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    Regulation of blood glucose by hypothalamic pyruvate metabolism (2005)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2005-08-06
    Description: The brain keenly depends on glucose for energy, and mammalians have redundant systems to control glucose production. An increase in circulating glucose inhibits glucose production in the liver, but this negative feedback is impaired in type 2 diabetes. Here we report that a primary increase in hypothalamic glucose levels lowers blood glucose through inhibition of glucose production in rats. The effect of glucose requires its conversion to lactate followed by stimulation of pyruvate metabolism, which leads to activation of adenosine triphosphate (ATP)-sensitive potassium channels. Thus, interventions designed to enhance the hypothalamic sensing of glucose may improve glucose homeostasis in diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lam, Tony K T -- Gutierrez-Juarez, Roger -- Pocai, Alessandro -- Rossetti, Luciano -- AG 21654/AG/NIA NIH HHS/ -- DK 20541/DK/NIDDK NIH HHS/ -- DK 45024/DK/NIDDK NIH HHS/ -- DK 48321/DK/NIDDK NIH HHS/ -- T32-AG023475/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2005 Aug 5;309(5736):943-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Departments of Medicine and Molecular Pharmacology, Diabetes Research Center, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16081739" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytes/metabolism ; Blood Glucose/*metabolism ; Citric Acid Cycle ; Feedback, Physiological ; Glucose/administration & dosage/*metabolism ; Glucose-6-Phosphatase/metabolism ; Hypothalamus/*metabolism ; Injections, Intraventricular ; Lactic Acid/metabolism ; Liver/*metabolism ; Male ; Neurons/metabolism ; Potassium Channels/metabolism ; Pyruvates/*metabolism ; Rats ; Rats, Sprague-Dawley
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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