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  • Articles  (71)
  • Rats  (70)
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  • Inorganic Chemistry
  • 1995-1999  (71)
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  • 1997  (71)
  • Physics  (71)
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  • Articles  (71)
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  • 1995-1999  (71)
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  • 1
    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
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  • 2
    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
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  • 3
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    American Association for the Advancement of Science (AAAS)
    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
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  • 4
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    American Association for the Advancement of Science (AAAS)
    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
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  • 5
    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
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  • 6
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    American Association for the Advancement of Science (AAAS)
    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
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  • 7
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    American Association for the Advancement of Science (AAAS)
    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
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  • 8
    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
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  • 9
    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
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  • 10
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    American Association for the Advancement of Science (AAAS)
    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
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  • 11
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    American Association for the Advancement of Science (AAAS)
    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
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  • 12
    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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  • 13
    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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  • 14
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    American Association for the Advancement of Science (AAAS)
    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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  • 15
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    American Association for the Advancement of Science (AAAS)
    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
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  • 16
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    American Association for the Advancement of Science (AAAS)
    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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    American Association for the Advancement of Science (AAAS)
    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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    American Association for the Advancement of Science (AAAS)
    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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    American Association for the Advancement of Science (AAAS)
    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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    American Association for the Advancement of Science (AAAS)
    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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  • 21
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    American Association for the Advancement of Science (AAAS)
    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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  • 22
    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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  • 23
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    American Association for the Advancement of Science (AAAS)
    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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  • 24
    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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    American Association for the Advancement of Science (AAAS)
    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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    American Association for the Advancement of Science (AAAS)
    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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  • 27
    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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  • 28
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    American Association for the Advancement of Science (AAAS)
    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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  • 29
    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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  • 30
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    American Association for the Advancement of Science (AAAS)
    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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  • 31
    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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  • 32
    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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  • 33
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    American Association for the Advancement of Science (AAAS)
    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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  • 34
    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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  • 35
    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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  • 36
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    American Association for the Advancement of Science (AAAS)
    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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  • 37
    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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  • 38
    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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  • 39
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    American Association for the Advancement of Science (AAAS)
    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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  • 40
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    American Association for the Advancement of Science (AAAS)
    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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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-10-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Potera, C -- New York, N.Y. -- Science. 1997 Oct 10;278(5336):225-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9340769" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Eukaryota/*growth & development/isolation & purification ; Fish Diseases/diagnosis/*parasitology ; Fisheries ; Montana ; Oligochaeta/parasitology ; Oncorhynchus mykiss/*parasitology ; Polymerase Chain Reaction ; Protozoan Infections/diagnosis/parasitology ; *Protozoan Infections, Animal ; RNA, Protozoan/genetics ; RNA, Ribosomal/genetics ; Spores/physiology ; Temperature
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  • 42
    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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  • 43
    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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  • 44
    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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  • 45
    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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  • 46
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    American Association for the Advancement of Science (AAAS)
    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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  • 47
    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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  • 48
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    American Association for the Advancement of Science (AAAS)
    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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  • 49
    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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  • 50
    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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  • 51
    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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  • 52
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    American Association for the Advancement of Science (AAAS)
    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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  • 53
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    American Association for the Advancement of Science (AAAS)
    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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  • 54
    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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  • 55
    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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  • 56
    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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  • 57
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    American Association for the Advancement of Science (AAAS)
    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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  • 58
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    American Association for the Advancement of Science (AAAS)
    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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  • 59
    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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  • 60
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    American Association for the Advancement of Science (AAAS)
    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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  • 61
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    American Association for the Advancement of Science (AAAS)
    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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  • 62
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    American Association for the Advancement of Science (AAAS)
    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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  • 63
    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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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 64
    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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  • 65
    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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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-08-08
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gura, T -- New York, N.Y. -- Science. 1997 Aug 8;277(5327):768.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9273698" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Apoptosis Regulatory Proteins ; Binding Sites ; Databases, Factual ; GPI-Linked Proteins ; Humans ; Membrane Glycoproteins/*metabolism/therapeutic use ; Neoplasms/*metabolism/pathology ; Rats ; Receptors, TNF-Related Apoptosis-Inducing Ligand ; Receptors, Tumor Necrosis Factor/chemistry/*metabolism ; TNF-Related Apoptosis-Inducing Ligand ; Tumor Cells, Cultured ; Tumor Necrosis Factor Decoy Receptors ; Tumor Necrosis Factor-alpha/*metabolism/therapeutic use
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  • 67
    Publication Date: 1997-10-23
    Description: The site of impulse initiation is crucial for the integrative actions of mammalian central neurons, but this question is currently controversial. Some recent studies support classical evidence that the impulse always arises in the soma-axon hillock region, with back-propagation through excitable dendrites, whereas others indicate that the dendrites are sufficiently excitable to initiate impulses that propagate forward along the dendrite to the soma-axon hillock. This issue has been addressed in the olfactory mitral cell, in which excitatory synaptic input is restricted to the distal tuft of a single primary dendrite. In rat olfactory bulb slices, dual whole cell recordings were made at or near the soma and from distal sites on the primary dendrite. The results show that the impulse can be initiated in either the soma-axon hillock or in the distal primary dendrite, and that the initiation site is controlled physiologically by the excitatory synaptic inputs to the distal tuft and inhibitory synaptic inputs near the soma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, W R -- Midtgaard, J -- Shepherd, G M -- New York, N.Y. -- Science. 1997 Oct 17;278(5337):463-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9334305" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Dendrites/*physiology ; Electric Stimulation ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; In Vitro Techniques ; Olfactory Bulb/*cytology/physiology ; Patch-Clamp Techniques ; Pyramidal Cells/*physiology ; Rats ; Rats, Sprague-Dawley ; Synapses/*physiology
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  • 68
    Publication Date: 1997-06-27
    Description: The effects of the active ingredient of Cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), and of the highly addictive drug heroin on in vivo dopamine transmission in the nucleus accumbens were compared in Sprague-Dawley rats by brain microdialysis. Delta9-THC and heroin increased extracellular dopamine concentrations selectively in the shell of the nucleus accumbens; these effects were mimicked by the synthetic cannabinoid agonist WIN55212-2. SR141716A, an antagonist of central cannabinoid receptors, prevented the effects of Delta9-THC but not those of heroin. Naloxone, a generic opioid antagonist, administered systemically, or naloxonazine, an antagonist of micro1 opioid receptors, infused into the ventral tegmentum, prevented the action of cannabinoids and heroin on dopamine transmission. Thus, Delta9-THC and heroin exert similar effects on mesolimbic dopamine transmission through a common mu1 opioid receptor mechanism located in the ventral mesencephalic tegmentum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tanda, G -- Pontieri, F E -- Di Chiara, G -- New York, N.Y. -- Science. 1997 Jun 27;276(5321):2048-50.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Toxicology and Consiglio Nazionale delle Ricerche (CNR), Center for Neuropharmacology, University of Cagliari, Viale A. Diaz 182, 09126 Cagliari, Italy.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9197269" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzoxazines ; Dopamine/*metabolism ; Dronabinol/antagonists & inhibitors/*pharmacology ; Heroin/*pharmacology ; Male ; Microdialysis ; Morpholines/antagonists & inhibitors/pharmacology ; Naloxone/analogs & derivatives/pharmacology ; Naphthalenes/antagonists & inhibitors/pharmacology ; Narcotic Antagonists/pharmacology ; Nucleus Accumbens/*drug effects/metabolism ; Piperidines/pharmacology ; Pyrazoles/pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, Cannabinoid ; Receptors, Drug/antagonists & inhibitors/metabolism ; Receptors, Opioid, mu/antagonists & inhibitors/*metabolism
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  • 69
    Publication Date: 1997-02-07
    Description: Glial cell line-derived neurotrophic factor (GDNF) supports growth and survival of dopaminergic (DA) neurons. A replication-defective adenoviral (Ad) vector encoding human GDNF injected near the rat substantia nigra was found to protect DA neurons from the progressive degeneration induced by the neurotoxin 6-hydroxydopamine (6-OHDA) injected into the striatum. Ad GDNF gene therapy reduced loss of DA neurons approximately threefold 6 weeks after 6-OHDA lesion, as compared with no treatment or injection of Ad lacZ or Ad mGDNF (encoding a biologically inactive deletion mutant GDNF). These results suggest that Ad vector-mediated GDNF gene therapy may slow the DA neuronal cell loss in humans with Parkinson's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Choi-Lundberg, D L -- Lin, Q -- Chang, Y N -- Chiang, Y L -- Hay, C M -- Mohajeri, H -- Davidson, B L -- Bohn, M C -- NS31957/NS/NINDS NIH HHS/ -- T32AG00107/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1997 Feb 7;275(5301):838-41.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology and Anatomy, University of Rochester, Box 603, 601 Elmwood Avenue, Rochester, NY 14642, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9012352" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics ; Animals ; Corpus Striatum/metabolism/pathology ; Dopamine/*physiology ; Gene Expression ; *Genetic Therapy ; Genetic Vectors ; Glial Cell Line-Derived Neurotrophic Factor ; Humans ; Male ; Molecular Sequence Data ; *Nerve Degeneration ; *Nerve Growth Factors ; Nerve Tissue Proteins/*genetics ; Neurons/pathology/physiology ; *Neuroprotective Agents ; Oxidopamine ; PC12 Cells ; Parkinson Disease/pathology/*therapy ; Rats ; Rats, Inbred F344 ; Substantia Nigra/metabolism/pathology ; Transgenes
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  • 70
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1997-09-12
    Description: In the developing nervous system, glial cells guide axons to their target areas, but it is unknown whether they help neurons to establish functional synaptic connections. The role of glial cells in synapse formation and function was studied in cultures of purified neurons from the rat central nervous system. In glia-free cultures, retinal ganglion cells formed synapses with normal ultrastructure but displayed little spontaneous synaptic activity and high failure rates in evoked synaptic transmission. In cocultures with neuroglia, the frequency and amplitude of spontaneous postsynaptic currents were potentiated by 70-fold and 5-fold, respectively, and fewer transmission failures occurred. Glial cells increased the action potential-independent quantal release by 12-fold without affecting neuronal survival. Thus, developing neurons in culture form inefficient synapses that require glial signals to become fully functional.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pfrieger, F W -- Barres, B A -- New York, N.Y. -- Science. 1997 Sep 12;277(5332):1684-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Stanford University, School of Medicine, Sherman Fairchild Science Building, 299 Campus Drive, Stanford, CA 94305-5125, USA. fpfrieg@mdc-berlin.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9287225" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Astrocytes/physiology ; Cell Survival ; Cells, Cultured ; Coculture Techniques ; Microglia/physiology ; Neuroglia/*physiology ; Oligodendroglia/physiology ; Rats ; Rats, Sprague-Dawley ; Retinal Ganglion Cells/cytology/*physiology/ultrastructure ; Synapses/*physiology/ultrastructure ; *Synaptic Transmission
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  • 71
    Publication Date: 1997-01-03
    Description: Regional brain activation was assessed by mapping of Fos-related protein expression in rats trained to self-administration of intravenous nicotine and cocaine. Both drugs produced specific overlapping patterns of activation in the shell and the core of the nucleus accumbens, medial prefrontal cortex, and medial caudate areas, but not in the amygdala. Thus, the reinforcing properties of cocaine and nicotine map on selected structures of the terminal fields of the mesocorticolimbic dopamine system, supporting the idea that common substrates for these addictive drugs exist.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pich, E M -- Pagliusi, S R -- Tessari, M -- Talabot-Ayer, D -- Hooft van Huijsduijnen, R -- Chiamulera, C -- New York, N.Y. -- Science. 1997 Jan 3;275(5296):83-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Geneva Biomedical Research Institute, Glaxo-Wellcome R&D, CH-1228 Geneva, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8974398" target="_blank"〉PubMed〈/a〉
    Keywords: Amygdala/drug effects/metabolism ; Animals ; Brain/*drug effects/metabolism ; Brain Mapping ; Cocaine/administration & dosage/*pharmacology ; DNA/metabolism ; Neostriatum/drug effects/metabolism ; Neurons/drug effects/metabolism ; Nicotine/administration & dosage/*pharmacology ; Nucleus Accumbens/drug effects/metabolism ; Opioid-Related Disorders/*etiology ; Prefrontal Cortex/drug effects/metabolism ; Proto-Oncogene Proteins c-fos/biosynthesis ; Rats ; Reinforcement (Psychology) ; Self Administration ; Substance-Related Disorders/*etiology ; Transcription Factor AP-1/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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