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  • Rats  (214)
  • American Association for the Advancement of Science (AAAS)  (214)
  • American Institute of Physics
  • 1995-1999  (64)
  • 1980-1984  (150)
  • 1925-1929
  • 1998  (64)
  • 1983  (150)
Collection
Publisher
  • American Association for the Advancement of Science (AAAS)  (214)
  • American Institute of Physics
  • Springer  (2)
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  • 1995-1999  (64)
  • 1980-1984  (150)
  • 1925-1929
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-28
    Description: The metabotropic glutamate receptors (mGluRs) are widely distributed in the brain and play important roles in synaptic plasticity. Here it is shown that some types of mGluRs are activated not only by glutamate but also by extracellular Ca2+ (Ca2+o). A single amino acid residue was found to determine the sensitivity of mGluRs to Ca2+o. One of the receptors, mGluR1alpha, but not its point mutant with reduced sensitivity to Ca2+o, caused morphological changes when transfected into mammalian cells. Thus, the sensing of Ca2+o by mGluRs may be important in cells under physiological condition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kubo, Y -- Miyashita, T -- Murata, Y -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1722-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurophysiology, Tokyo Metropolitan Institute for Neuroscience, Musashidai 2-6, Fuchu, Tokyo 183-8526, Japan. ykubo@tmin.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497291" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/ultrastructure ; Amino Acid Sequence ; Animals ; Binding Sites ; Brain/metabolism ; CHO Cells ; Calcium/*metabolism/pharmacology ; Cell Size ; Cricetinae ; Cyclic AMP/metabolism ; G Protein-Coupled Inwardly-Rectifying Potassium Channels ; Glutamic Acid/metabolism/pharmacology ; Molecular Sequence Data ; Oocytes ; Point Mutation ; Potassium Channels/metabolism ; *Potassium Channels, Inwardly Rectifying ; Rats ; Receptors, Metabotropic Glutamate/chemistry/genetics/*metabolism ; Recombinant Fusion Proteins/metabolism ; Second Messenger Systems ; Transfection ; Xenopus laevis
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  • 2
    Publication Date: 1998-08-07
    Description: Clathrin-mediated endocytosis involves cycles of assembly and disassembly of clathrin coat components and their accessory proteins. Dephosphorylation of rat brain extract was shown to promote the assembly of dynamin 1, synaptojanin 1, and amphiphysin into complexes that also included clathrin and AP-2. Phosphorylation of dynamin 1 and synaptojanin 1 inhibited their binding to amphiphysin, whereas phosphorylation of amphiphysin inhibited its binding to AP-2 and clathrin. Thus, phosphorylation regulates the association and dissociation cycle of the clathrin-based endocytic machinery, and calcium-dependent dephosphorylation of endocytic proteins could prepare nerve terminals for a burst of endocytosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Slepnev, V I -- Ochoa, G C -- Butler, M H -- Grabs, D -- De Camilli, P -- CA46128/CA/NCI NIH HHS/ -- NS36251/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):821-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute and Department of Cell Biology, Yale University School of Medicine, 295 Congress Avenue, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9694653" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptor Protein Complex alpha Subunits ; Adaptor Protein Complex beta Subunits ; Adaptor Proteins, Vesicular Transport ; Adenosine Triphosphate/metabolism ; Animals ; Binding Sites ; Carbazoles/pharmacology ; Chromatography, Affinity ; Clathrin/*metabolism ; Cyclosporine/pharmacology ; Dimerization ; Dynamin I ; Dynamins ; *Endocytosis ; Enzyme Inhibitors/pharmacology ; GTP Phosphohydrolases/*metabolism ; Indole Alkaloids ; Membrane Proteins/*metabolism ; Nerve Tissue Proteins/*metabolism ; Phosphoric Monoester Hydrolases/*metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; src Homology Domains
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  • 3
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-08-14
    Description: Differential actions of acetylcholine on the excitability of two subtypes of interneurons in layer V of the rat visual cortex were examined. Acetylcholine excited low-threshold spike (LTS) cells through nicotinic receptors, whereas it elicited hyperpolarization in fast spiking (FS) cells through muscarinic receptors. Axons of LTS cells were mainly distributed vertically to upper layers, and those of FS cells were primarily confined to layer V. Thus, cortical cholinergic activation may reduce some forms of intralaminar inhibition, promote intracolumnar inhibition, and change the direction of information flow within cortical circuits.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xiang, Z -- Huguenard, J R -- Prince, D A -- NS 06477/NS/NINDS NIH HHS/ -- NS 07280/NS/NINDS NIH HHS/ -- NS 12151/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Aug 14;281(5379):985-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurology and Neurological Sciences, Stanford University Medical Center, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9703513" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/*physiology ; Animals ; Hexamethonium/pharmacology ; In Vitro Techniques ; Interneurons/physiology ; Membrane Potentials ; Muscarinic Antagonists/pharmacology ; Nerve Net/*physiology ; *Neural Inhibition ; Nicotinic Antagonists/pharmacology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Nicotinic/physiology ; Scopolamine Hydrobromide/pharmacology ; Visual Cortex/cytology/*physiology
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  • 4
    Publication Date: 1998-02-21
    Description: Protein kinase B (PKB) is activated in response to phosphoinositide 3-kinases and their lipid products phosphatidylinositol 3,4, 5-trisphosphate [PtdIns(3,4,5)P3] and PtdIns(3,4)P2 in the signaling pathways used by a wide variety of growth factors, antigens, and inflammatory stimuli. PKB is a direct target of these lipids, but this regulation is complex. The lipids can bind to the pleckstrin homologous domain of PKB, causing its translocation to the membrane, and also enable upstream, Thr308-directed kinases to phosphorylate and activate PKB. Four isoforms of these PKB kinases were purified from sheep brain. They bound PtdIns(3,4,5)P3 and associated with lipid vesicles containing it. These kinases contain an NH2-terminal catalytic domain and a COOH-terminal pleckstrin homologous domain, and their heterologous expression augments receptor activation of PKB, which suggests they are the primary signal transducers that enable PtdIns(3,4,5)P3 or PtdIns- (3,4)P2 to activate PKB and hence to control signaling pathways regulating cell survival, glucose uptake, and glycogen metabolism.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stephens, L -- Anderson, K -- Stokoe, D -- Erdjument-Bromage, H -- Painter, G F -- Holmes, A B -- Gaffney, P R -- Reese, C B -- McCormick, F -- Tempst, P -- Coadwell, J -- Hawkins, P T -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):710-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Inositide Laboratory, The Babraham Institute, Babraham, Cambridge CB2 4AT, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445477" target="_blank"〉PubMed〈/a〉
    Keywords: 3-Phosphoinositide-Dependent Protein Kinases ; Alternative Splicing ; Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/enzymology ; Cloning, Molecular ; DNA, Complementary ; Drosophila ; Drosophila Proteins ; Enzyme Activation ; Humans ; Liposomes/metabolism ; Molecular Sequence Data ; Open Reading Frames ; Phosphatidylinositol Phosphates/*metabolism ; Phosphorylation ; Platelet-Derived Growth Factor/pharmacology ; Protein-Serine-Threonine Kinases/chemistry/genetics/isolation & ; purification/*metabolism ; Proto-Oncogene Proteins/*metabolism ; Proto-Oncogene Proteins c-akt ; Rats ; Recombinant Proteins/metabolism ; Sheep ; *Signal Transduction
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  • 5
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-10-09
    Description: Differential access to cocaine self-administration produced two patterns of drug intake in rats. With 1 hour of access per session, drug intake remained low and stable. In contrast, with 6 hours of access, drug intake gradually escalated over days. After escalation, drug consumption was characterized by an increased early drug loading and an upward shift in the cocaine dose-response function, suggesting an increase in hedonic set point. After 1 month of abstinence, escalation of cocaine intake was reinstated to a higher level than before. These findings may provide an animal model for studying the development of excessive drug intake and the basis of addiction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmed, S H -- Koob, G F -- DA04398/DA/NIDA NIH HHS/ -- DA08467/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):298-300.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Psychopharmacology, Department of Neuropharmacology, CVN-7, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. aserge@sage.scripps.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765157" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Behavior, Addictive ; Cocaine/*administration & dosage ; Cocaine-Related Disorders/*etiology ; Dose-Response Relationship, Drug ; Drug Tolerance ; Male ; Rats ; Rats, Wistar ; Reinforcement (Psychology) ; Time Factors
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  • 6
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-21
    Description: Mossy fiber synaptic transmission at hippocampal CA3 pyramidal cells and interneurons was compared in rat brain slices to determine whether mossy terminals are functionally equivalent. Tetanic stimulation of mossy fibers induced long-term potentiation in pyramidal neurons but was either without effect or it induced depression at synapses onto interneurons. Unlike transmission onto pyramidal neurons, transmission onto interneurons was not potentiated after adenosine 3',5'-monophosphate (cAMP) activation. Furthermore, metabotropic glutamate receptor depression of transmission onto interneurons did not involve cAMP-dependent pathways. Thus, synaptic terminals arising from a common afferent pathway do not function as a single compartment but are specialized, depending on their postsynaptic target.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Maccaferri, G -- Toth, K -- McBain, C J -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1368-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cellular and Molecular Neurophysiology, Room 5A72, Building 49, National Institute of Child Health and Human Development, 9000 Rockville Pike, Bethesda MD 20892-4495, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478900" target="_blank"〉PubMed〈/a〉
    Keywords: Afferent Pathways ; Animals ; Colforsin/pharmacology ; Cyclic AMP/metabolism ; Cycloleucine/analogs & derivatives/pharmacology ; Cyclopropanes/pharmacology ; Electric Stimulation ; Excitatory Postsynaptic Potentials/drug effects ; Glycine/analogs & derivatives/pharmacology ; Hippocampus/cytology/*physiology ; In Vitro Techniques ; Interneurons/drug effects/*physiology ; *Long-Term Potentiation ; Mossy Fibers, Hippocampal/*physiology ; Pyramidal Cells/drug effects/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/agonists/physiology ; Synaptic Transmission/drug effects
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  • 7
    Publication Date: 1998-03-21
    Description: Long-term potentiation (LTP) is an activity-dependent strengthening of synaptic efficacy that is considered to be a model of learning and memory. Protein tyrosine phosphorylation is necessary to induce LTP. Here, induction of LTP in CA1 pyramidal cells of rats was prevented by blocking the tyrosine kinase Src, and Src activity was increased by stimulation producing LTP. Directly activating Src in the postsynaptic neuron enhanced excitatory synaptic responses, occluding LTP. Src-induced enhancement of alpha-amino-3-hydroxy-5-methylisoxazolepropionic acid (AMPA) receptor-mediated synaptic responses required raised intracellular Ca2+ and N-methyl-D-aspartate (NMDA) receptors. Thus, Src activation is necessary and sufficient for inducing LTP and may function by up-regulating NMDA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lu, Y M -- Roder, J C -- Davidow, J -- Salter, M W -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1363-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Samuel Lunenfeld Research Institute, Mount Sinai Hospital, and Department of Molecular and Medical Genetics, University of Toronto, M5S 1A8, Canada.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478899" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/metabolism ; Electric Stimulation ; Enzyme Activation ; Excitatory Postsynaptic Potentials/drug effects ; Hippocampus/cytology/enzymology/*physiology ; In Vitro Techniques ; *Long-Term Potentiation ; Molecular Sequence Data ; Oligopeptides/pharmacology ; Patch-Clamp Techniques ; Peptide Fragments/pharmacology ; Proto-Oncogene Proteins pp60(c-src)/pharmacology ; Pyramidal Cells/enzymology/*physiology ; Rats ; Rats, Sprague-Dawley ; Receptors, AMPA/physiology ; Receptors, N-Methyl-D-Aspartate/physiology ; Recombinant Proteins/pharmacology ; Up-Regulation ; src-Family Kinases/*metabolism
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  • 8
    Publication Date: 1998-09-11
    Description: Leptin is a hormone that regulates food intake, and its receptor (OB-Rb) is expressed primarily in the hypothalamus. Here, it is shown that OB-Rb is also expressed in human vasculature and in primary cultures of human endothelial cells. In vitro and in vivo assays revealed that leptin has angiogenic activity. In vivo, leptin induced neovascularization in corneas from normal rats but not in corneas from fa/fa Zucker rats, which lack functional leptin receptors. These observations indicate that the vascular endothelium is a target for leptin and suggest a physiological mechanism whereby leptin-induced angiogenesis may facilitate increased energy expenditure.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sierra-Honigmann, M R -- Nath, A K -- Murakami, C -- Garcia-Cardena, G -- Papapetropoulos, A -- Sessa, W C -- Madge, L A -- Schechner, J S -- Schwabb, M B -- Polverini, P J -- Flores-Riveros, J R -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1683-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Boyer Center for Molecular Medicine, Yale University School of Medicine, New Haven, CT 06536, USA. rocio_sierra-honigmann@qm.yale.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733517" target="_blank"〉PubMed〈/a〉
    Keywords: Adipocytes/metabolism ; Amino Acid Sequence ; Animals ; Carrier Proteins/analysis/*physiology ; Cells, Cultured ; Corneal Neovascularization ; DNA-Binding Proteins/metabolism ; Endothelial Growth Factors/pharmacology ; Endothelium, Vascular/chemistry/cytology/*physiology ; Energy Metabolism ; Humans ; Leptin ; Lipid Metabolism ; Lymphokines/pharmacology ; Molecular Sequence Data ; *Neovascularization, Physiologic ; Phosphorylation ; Proteins/pharmacology/*physiology ; Rats ; Rats, Zucker ; *Receptors, Cell Surface ; Receptors, Leptin ; STAT3 Transcription Factor ; Trans-Activators/metabolism ; Vascular Endothelial Growth Factor A ; Vascular Endothelial Growth Factors
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  • 9
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sikorski, R -- Peters, R -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1438.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867652" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/virology ; Genetic Therapy/*methods ; *Genetic Vectors ; HIV/*genetics/physiology ; Neurons/virology ; Rats ; Retina/virology
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  • 10
    Publication Date: 1998-12-18
    Description: Cocaine regulates the transcription factor CREB (adenosine 3', 5'-monophosphate response element binding protein) in rat nucleus accumbens, a brain region that is important for addiction. Overexpression of CREB in this region decreases the rewarding effects of cocaine and makes low doses of the drug aversive. Conversely, overexpression of a dominant-negative mutant CREB increases the rewarding effects of cocaine. Altered transcription of dynorphin likely contributes to these effects: Its expression is increased by overexpression of CREB and decreased by overexpression of mutant CREB. Moreover, blockade of kappa opioid receptors (on which dynorphin acts) antagonizes the negative effect of CREB on cocaine reward. These results identify an intracellular cascade-culminating in gene expression-through which exposure to cocaine modifies subsequent responsiveness to the drug.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlezon, W A Jr -- Thome, J -- Olson, V G -- Lane-Ladd, S B -- Brodkin, E S -- Hiroi, N -- Duman, R S -- Neve, R L -- Nestler, E J -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2272-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Psychiatry, Center for Genes and Behavior, Yale University School of Medicine and Connecticut Mental Health Center, New Haven, CT 06508, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856954" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/administration & dosage/*pharmacology ; Conditioning (Psychology) ; Cyclic AMP Response Element-Binding Protein/genetics/*metabolism ; Dose-Response Relationship, Drug ; Dynorphins/genetics/metabolism ; Gene Expression ; Gene Expression Regulation ; Gene Transfer Techniques ; Genetic Vectors ; Naltrexone/analogs & derivatives/pharmacology ; Narcotic Antagonists/pharmacology ; Neurons/metabolism ; Nucleus Accumbens/*metabolism ; Point Mutation ; RNA, Messenger/genetics/metabolism ; Rats ; Receptors, Opioid, kappa/antagonists & inhibitors/metabolism ; *Reward ; Simplexvirus/genetics
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  • 11
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-05-09
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawler, A -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):515-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9575093" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Nervous System Physiological Phenomena ; Rats ; *Research ; Space Flight ; *Spacecraft ; United States ; United States National Aeronautics and Space Administration ; *Weightlessness
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  • 12
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-05-09
    Description: Many molecular mechanisms for neural adaptation to stress remain unknown. Expression of alternative splice variants of Slo, a gene encoding calcium- and voltage-activated potassium channels, was measured in rat adrenal chromaffin tissue from normal and hypophysectomized animals. Hypophysectomy triggered an abrupt decrease in the proportion of Slo transcripts containing a "STREX" exon. The decrease was prevented by adrenocorticotropic hormone injections. In Xenopus oocytes, STREX variants produced channels with functional properties associated with enhanced repetitive firing. Thus, the hormonal stress axis is likely to control the excitable properties of epinephrine-secreting cells by regulating alternative splicing of Slo messenger RNA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Xie, J -- McCobb, D P -- New York, N.Y. -- Science. 1998 Apr 17;280(5362):443-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section of Neurobiology and Behavior, Cornell University, Ithaca, NY 14853, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9545224" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Medulla/*metabolism ; Adrenocorticotropic Hormone/metabolism/*pharmacology ; *Alternative Splicing ; Amino Acid Sequence ; Animals ; Chromaffin Cells/*metabolism ; Corticosterone/blood/*metabolism ; Dexamethasone/pharmacology ; Epinephrine/secretion ; Exons ; Female ; Hypophysectomy ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Large-Conductance Calcium-Activated Potassium Channels ; Male ; Molecular Sequence Data ; Oocytes ; Phenylethanolamine N-Methyltransferase/genetics ; Polymerase Chain Reaction ; Potassium Channels/*genetics ; *Potassium Channels, Calcium-Activated ; RNA, Messenger/genetics/metabolism ; Rats ; Rats, Sprague-Dawley ; Xenopus
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  • 13
    Publication Date: 1998-09-04
    Description: Nerve growth is regulated by attractive and repulsive factors in the nervous system. Microscopic gradients of Collapsin-1/Semaphorin III/D (Sema III) and myelin-associated glycoprotein trigger repulsive turning responses by growth cones of cultured Xenopus spinal neurons; the repulsion can be converted to attraction by pharmacological activation of the guanosine 3',5'-monophosphate (cGMP) and adenosine 3',5'-monophosphate signaling pathways, respectively. Sema III also causes the collapse of cultured rat sensory growth cones, which can be inhibited by activation of the cGMP pathway. Thus cyclic nucleotides can regulate growth cone behaviors and may be targets for designing treatments to alleviate the inhibition of nerve regeneration by repulsive factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Song, H -- Ming, G -- He, Z -- Lehmann, M -- McKerracher, L -- Tessier-Lavigne, M -- Poo, M -- NS22764/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 4;281(5382):1515-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of California at San Diego, La Jolla, CA 92093-0357, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9727979" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Calcium/physiology ; Cells, Cultured ; Cyclic AMP/analogs & derivatives/pharmacology/*physiology ; Cyclic GMP/analogs & derivatives/pharmacology/*physiology ; Ganglia, Spinal/cytology ; Glycoproteins/*physiology ; Myelin-Associated Glycoprotein/physiology ; Nerve Growth Factors/*physiology ; Nerve Tissue Proteins/physiology ; Neurites/*physiology ; Neurons/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins ; Semaphorin-3A ; Spinal Cord/cytology ; Thionucleotides/pharmacology ; Xenopus
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  • 14
    Publication Date: 1998-01-31
    Description: Candidate mammalian odorant receptors were first cloned some 6 years ago. The physiological function of these receptors in initiating transduction in olfactory receptor neurons remains to be established. Here, a recombinant adenovirus was used to drive expression of a particular receptor gene in an increased number of sensory neurons in the rat olfactory epithelium. Electrophysiological recording showed that increased expression of a single gene led to greater sensitivity to a small subset of odorants.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhao, H -- Ivic, L -- Otaki, J M -- Hashimoto, M -- Mikoshiba, K -- Firestein, S -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):237-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Interdepartmental Neuroscience Program, Yale University, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9422698" target="_blank"〉PubMed〈/a〉
    Keywords: Adenoviridae/genetics/physiology ; Aldehydes/metabolism/*pharmacology ; Animals ; Electrophysiology ; Female ; Gene Expression ; Genetic Vectors ; Green Fluorescent Proteins ; Luminescent Proteins/analysis/genetics ; Male ; *Odors ; Olfactory Receptor Neurons/*physiology/virology ; Patch-Clamp Techniques ; Rats ; Rats, Sprague-Dawley ; Receptors, Odorant/genetics/metabolism/*physiology ; Recombinant Proteins
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  • 15
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-29
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1998 Nov 20;282(5393):1439.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9867653" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Binding Sites ; Cattle ; Cyclic GMP/chemistry/*metabolism ; Cyclic GMP-Dependent Protein Kinase Type I ; Cyclic GMP-Dependent Protein Kinases/chemistry/*metabolism ; Dimerization ; Ion Channel Gating ; Ion Channels/chemistry/*metabolism ; Ligands ; Polyethylene Glycols ; Rats ; Retinal Rod Photoreceptor Cells/metabolism
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  • 16
    Publication Date: 1998-09-11
    Description: Hypertrophic cardiomyopathy (HCM) is an inherited form of heart disease that affects 1 in 500 individuals. Here it is shown that calcineurin, a calcium-regulated phosphatase, plays a critical role in the pathogenesis of HCM. Administration of the calcineurin inhibitors cyclosporin and FK506 prevented disease in mice that were genetically predisposed to develop HCM as a result of aberrant expression of tropomodulin, myosin light chain-2, or fetal beta-tropomyosin in the heart. Cyclosporin had a similar effect in a rat model of pressure-overload hypertrophy. These results suggest that calcineurin inhibitors merit investigation as potential therapeutics for certain forms of human heart disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sussman, M A -- Lim, H W -- Gude, N -- Taigen, T -- Olson, E N -- Robbins, J -- Colbert, M C -- Gualberto, A -- Wieczorek, D F -- Molkentin, J D -- HL58224-01/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Sep 11;281(5383):1690-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Molecular Cardiovascular Biology, Children's Hospital Medical Center, 3333 Burnet Avenue, Cincinnati, OH 45229, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9733519" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcineurin/metabolism ; *Calcineurin Inhibitors ; Calcium/metabolism ; *Cardiac Myosins ; Cardiomegaly/metabolism/pathology/*prevention & control ; Cardiomyopathy, Dilated/pathology/*prevention & control ; Cardiomyopathy, Hypertrophic/genetics/metabolism/pathology/*prevention & control ; Carrier Proteins/genetics ; Cyclosporine/*pharmacology ; Female ; Mice ; Mice, Transgenic ; *Microfilament Proteins ; Models, Cardiovascular ; Myocardium/*metabolism/pathology ; Myosin Light Chains/genetics/metabolism ; Rats ; Signal Transduction ; Tacrolimus/*pharmacology ; Tropomodulin ; Tropomyosin/genetics
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  • 17
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-07
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanck, D -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1004.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Chicago, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9490476" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/*metabolism ; Calcium Channels/*metabolism ; Ion Channel Gating ; Muscle, Skeletal/metabolism ; Myocardial Contraction/*physiology ; Myocardium/*metabolism ; Rats ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcolemma/metabolism ; Sarcoplasmic Reticulum/metabolism ; Sodium Channels/*metabolism
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  • 18
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicoll, R A -- Malenka, R C -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):360-1.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Pharmacology, University of California, San Francisco, CA 94143-0450, USA. nicoll@phy.ucsf.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9705712" target="_blank"〉PubMed〈/a〉
    Keywords: *Amino Acid Transport Systems, Neutral ; Animals ; Carrier Proteins/metabolism ; GABA Plasma Membrane Transport Proteins ; Glycine/*metabolism ; Glycine Plasma Membrane Transport Proteins ; Interneurons/*metabolism ; Membrane Proteins/metabolism ; *Membrane Transport Proteins ; Motor Neurons/*metabolism ; *Organic Anion Transporters ; Presynaptic Terminals/*metabolism ; Rats ; Receptor Aggregation ; Receptors, GABA/metabolism ; Receptors, Glycine/metabolism ; Spinal Cord/cytology ; Synaptic Transmission ; Synaptic Vesicles/metabolism ; gamma-Aminobutyric Acid/*metabolism
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  • 19
    Publication Date: 1998-03-21
    Description: The nocturnal increase in circulating melatonin in vertebrates is regulated by 10- to 100-fold increases in pineal serotonin N-acetyltransferase (AA-NAT) activity. Changes in the amount of AA-NAT protein were shown to parallel changes in AA-NAT activity. When neural stimulation was switched off by either light exposure or L-propranolol-induced beta-adrenergic blockade, both AA-NAT activity and protein decreased rapidly. Effects of L-propranolol were blocked in vitro by dibutyryl adenosine 3',5'-monophosphate (cAMP) or inhibitors of proteasomal proteolysis. This result indicates that adrenergic-cAMP regulation of AA-NAT is mediated by rapid reversible control of selective proteasomal proteolysis. Similar proteasome-based mechanisms may function widely as selective molecular switches in vertebrate neural systems.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Gastel, J A -- Roseboom, P H -- Rinaldi, P A -- Weller, J L -- Klein, D C -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1358-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Section on Neuroendocrinology, Laboratory of Developmental Neurobiology, National Institute of Child Health and Human Development (NICHD), National Institutes of Health, Bethesda, MD 20892-4480, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9478897" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Adrenergic beta-Antagonists/pharmacology ; Animals ; Arylamine N-Acetyltransferase/*metabolism ; Bucladesine/pharmacology ; Cyclic AMP/metabolism ; Cysteine Endopeptidases/*metabolism ; Cysteine Proteinase Inhibitors/pharmacology ; Isoproterenol/pharmacology ; Light ; Melatonin/*biosynthesis ; Multienzyme Complexes/*metabolism ; Pineal Gland/cytology/drug effects/enzymology/*metabolism ; Propranolol/pharmacology ; Proteasome Endopeptidase Complex ; Rats ; Receptors, Adrenergic, beta/physiology
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  • 20
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-06-27
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pallini, R -- New York, N.Y. -- Science. 1998 Apr 10;280(5361):181-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9565524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology/*ultrastructure ; Brain Tissue Transplantation ; Cell Transplantation ; Denervation ; Myelin Sheath/physiology ; *Nerve Regeneration ; Neuroglia/physiology/*transplantation ; Olfactory Bulb/cytology ; Rats ; Schwann Cells/physiology ; Spinal Cord/cytology/*physiology ; Spinal Cord Injuries/pathology/*surgery
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  • 21
    Publication Date: 1998-02-21
    Description: There are several forms of hereditary human hair loss, known collectively as alopecias, the molecular bases of which are entirely unknown. A kindred with a rare, recessively inherited type of alopecia universalis was used to search for a locus by homozygosity mapping, and linkage was established in a 6-centimorgan interval on chromosome 8p12 (the logarithm of the odds favoring linkage score was 6.19). The human homolog of a murine gene, hairless, was localized in this interval by radiation hybrid mapping, and a missense mutation was found in affected individuals. Human hairless encodes a putative single zinc finger transcription factor protein with restricted expression in the brain and skin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ahmad, W -- Faiyaz ul Haque, M -- Brancolini, V -- Tsou, H C -- ul Haque, S -- Lam, H -- Aita, V M -- Owen, J -- deBlaquiere, M -- Frank, J -- Cserhalmi-Friedman, P B -- Leask, A -- McGrath, J A -- Peacocke, M -- Ahmad, M -- Ott, J -- Christiano, A M -- HG-00008/HG/NHGRI NIH HHS/ -- P30AR44535/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):720-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Dermatology, Columbia University, 630 West 168 Street, VC-15-526, New York, NY 10032, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445480" target="_blank"〉PubMed〈/a〉
    Keywords: Alopecia/*genetics ; Amino Acid Sequence ; Animals ; Brain/metabolism ; Chromosome Mapping ; Chromosomes, Human, Pair 8 ; DNA-Binding Proteins/genetics ; Female ; Forkhead Transcription Factors ; Gene Expression ; Genes, Recessive ; Homozygote ; Humans ; Male ; Mice ; Mice, Hairless/genetics ; Microsatellite Repeats ; Molecular Sequence Data ; Mutation ; Pedigree ; Proteins/chemistry/*genetics ; Rats ; Sequence Analysis, DNA ; Sequence Homology, Amino Acid ; Skin/metabolism ; Transcription Factors/genetics ; *Zinc Fingers
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  • 22
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-01-24
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Strauss, E -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):32-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9441405" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Non-Narcotic/chemical synthesis/chemistry/metabolism/*pharmacology ; Animals ; Anura ; Azetidines/chemical synthesis/chemistry/metabolism/*pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology/toxicity ; Drug Evaluation, Preclinical ; Nicotinic Agonists/chemistry/metabolism/pharmacology/toxicity ; Pain Measurement ; Pyridines/chemical synthesis/chemistry/metabolism/*pharmacology/toxicity ; Rats ; Receptors, Nicotinic/metabolism
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  • 23
    Publication Date: 1998-02-07
    Description: Mitogen stimulation of cytoskeletal changes and c-jun amino-terminal kinases is mediated by Rac small guanine nucleotide-binding proteins. Vav, a guanosine diphosphate (GDP)-guanosine triphosphate (GTP) exchange factor for Rac that stimulates the exchange of bound GDP for GTP, bound to and was directly controlled by substrates and products of phosphoinositide (PI) 3-kinase. The PI 3-kinase substrate phosphatidylinositol-4,5-bisphosphate inhibited activation of Vav by the tyrosine kinase Lck, whereas the product phosphatidylinositol-3,4,5-trisphosphate enhanced phosphorylation and activation of Vav by Lck. Control of Vav in response to mitogens by the products of PI 3-kinase suggests a mechanism for Ras-dependent activation of Rac.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Han, J -- Luby-Phelps, K -- Das, B -- Shu, X -- Xia, Y -- Mosteller, R D -- Krishna, U M -- Falck, J R -- White, M A -- Broek, D -- CA50261/CA/NCI NIH HHS/ -- CA71443/CA/NCI NIH HHS/ -- GM31278/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):558-60.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Molecular Biology, Norris Comprehensive Cancer Center, University of Southern California, Los Angeles, CA 90033-0800, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438848" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Enzyme Activation ; GTP Phosphohydrolases/*metabolism ; GTP-Binding Proteins/*metabolism ; Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/*metabolism ; Guanosine Triphosphate/metabolism ; Inositol 1,4,5-Trisphosphate/metabolism/pharmacology ; Lymphocyte Specific Protein Tyrosine Kinase p56(lck)/metabolism ; Mutagenesis, Site-Directed ; Oncogene Proteins/chemistry/*metabolism ; Phosphatidylinositol 3-Kinases/*metabolism ; Phosphatidylinositol 4,5-Diphosphate/metabolism/pharmacology ; Phosphatidylinositol Phosphates/metabolism/pharmacology ; Phosphatidylinositols/*metabolism/pharmacology ; Phosphorylation ; Proteins/metabolism ; Proto-Oncogene Proteins c-vav ; Rats ; rac GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors
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  • 24
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1302-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735048" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis/drug effects ; Brain/metabolism/*pathology ; Brain Ischemia/drug therapy/metabolism/pathology ; *Cell Death ; Cerebrovascular Disorders/drug therapy/metabolism/*pathology ; Cysteine Endopeptidases/metabolism ; Cysteine Proteinase Inhibitors/pharmacology/therapeutic use ; DNA Fragmentation ; Humans ; Mice ; Necrosis ; Neurons/metabolism/*pathology ; Rats
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  • 25
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reed, R R -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):193.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Molecular Biology and Genetics, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA. rreed@jhmi.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9446227" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Octanol/pharmacology ; Adenoviridae/genetics/physiology ; Animals ; Caenorhabditis elegans ; *Caenorhabditis elegans Proteins ; Electrophysiology ; Genetic Vectors ; Green Fluorescent Proteins ; Helminth Proteins/physiology ; Ligands ; Luminescent Proteins/analysis/genetics ; *Odors ; Olfactory Receptor Neurons/*physiology ; Patch-Clamp Techniques ; Rats ; Receptors, Odorant/genetics/*physiology ; Recombinant Proteins
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  • 26
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Feb 27;279(5355):1301.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508703" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carotid Body/*cytology/metabolism ; Cell Survival ; *Cell Transplantation ; Corpus Striatum/pathology ; Dopamine/biosynthesis/secretion ; Humans ; Nerve Fibers/ultrastructure ; Nerve Growth Factors/biosynthesis ; Neural Pathways ; Parkinson Disease/pathology/*surgery ; Rats ; Substantia Nigra/pathology
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  • 27
    Publication Date: 1998-12-04
    Description: The M-current regulates the subthreshold electrical excitability of many neurons, determining their firing properties and responsiveness to synaptic input. To date, however, the genes that encode subunits of this important channel have not been identified. The biophysical properties, sensitivity to pharmacological blockade, and expression pattern of the KCNQ2 and KCNQ3 potassium channels were determined. It is concluded that both these subunits contribute to the native M-current.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, H S -- Pan, Z -- Shi, W -- Brown, B S -- Wymore, R S -- Cohen, I S -- Dixon, J E -- McKinnon, D -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1890-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Molecular Cardiology, Department of Physiology and Biophysics, State University of New York at Stony Brook, Stony Brook, NY 11794, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9836639" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Anthracenes/pharmacology ; Brain/metabolism ; Ganglia, Sympathetic/metabolism ; Gene Expression ; Humans ; Indoles/pharmacology ; KCNQ2 Potassium Channel ; KCNQ3 Potassium Channel ; Kinetics ; Neurons/drug effects/physiology ; Oocytes ; Patch-Clamp Techniques ; Potassium/*metabolism ; Potassium Channels/chemistry/drug effects/genetics/*metabolism ; Potassium Channels, Voltage-Gated ; Pyridines/pharmacology ; Rats ; Sympathetic Nervous System/drug effects/physiology ; Tetraethylammonium/pharmacology ; Xenopus
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  • 28
    Publication Date: 1998-10-09
    Description: p53 acts as a tumor suppressor by inducing both growth arrest and apoptosis. p53-induced apoptosis can occur without new RNA synthesis through an unknown mechanism. In human vascular smooth muscle cells, p53 activation transiently increased surface Fas (CD95) expression by transport from the Golgi complex. Golgi disruption blocked both p53-induced surface Fas expression and apoptosis. p53 also induced Fas-FADD binding and transiently sensitized cells to Fas-induced apoptosis. In contrast, lpr and gld fibroblasts were resistant to p53-induced apoptosis. Thus, p53 can mediate apoptosis through Fas transport from cytoplasmic stores.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bennett, M -- Macdonald, K -- Chan, S W -- Luzio, J P -- Simari, R -- Weissberg, P -- HL34073/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1998 Oct 9;282(5387):290-3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of Cambridge, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9765154" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptor Proteins, Signal Transducing ; Animals ; Antigens, CD95/genetics/*metabolism ; *Apoptosis/drug effects ; Brefeldin A/pharmacology ; Carrier Proteins/metabolism ; Cell Membrane/*metabolism ; Cells, Cultured ; Enzyme Inhibitors/pharmacology ; Etoposide/pharmacology ; Fas Ligand Protein ; Fas-Associated Death Domain Protein ; Golgi Apparatus/metabolism ; Humans ; Membrane Glycoproteins/genetics/metabolism ; Mice ; Muscle, Smooth, Vascular/cytology ; Mutation ; Protein Synthesis Inhibitors/pharmacology ; Rats ; Topoisomerase II Inhibitors ; Tumor Suppressor Protein p53/*physiology
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  • 29
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Feb 20;279(5354):1134.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9508686" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Appetite/drug effects ; Appetite Stimulants/*isolation & purification/metabolism/pharmacology ; Hypothalamic Area, Lateral/chemistry/*physiology ; Nerve Tissue Proteins/*isolation & purification/metabolism/pharmacology ; Peptides/*isolation & purification/metabolism/pharmacology ; Rats ; Receptors, Cell Surface/metabolism ; Starvation
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  • 30
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Enserink, M -- New York, N.Y. -- Science. 1998 Aug 21;281(5380):1124-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735026" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Concanavalin A/genetics ; Crops, Agricultural/*adverse effects ; European Union ; *Genetic Engineering ; Great Britain ; Lectins/genetics ; Plant Lectins ; Plants, Genetically Modified/*adverse effects ; Rats ; Solanum tuberosum/*genetics
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  • 31
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-07-17
    Description: It is widely accepted that individual neurons in the central nervous system release only a single fast transmitter. The possibility of corelease of fast neurotransmitters was examined by making paired recordings from synaptically connected neurons in spinal cord slices. Unitary inhibitory postsynaptic currents generated at interneuron-motoneuron synapses consisted of a strychnine-sensitive, glycine receptor-mediated component and a bicuculline-sensitive, gamma-aminobutyric acid (GABA)A receptor-mediated component. These results indicate that spinal interneurons release both glycine and GABA to activate functionally distinct receptors in their postsynaptic target cells. A subset of miniature synaptic currents also showed both components, consistent with corelease from individual synaptic vesicles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jonas, P -- Bischofberger, J -- Sandkuhler, J -- New York, N.Y. -- Science. 1998 Jul 17;281(5375):419-24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Physiologisches Institut der Universitat Freiburg, D-79104 Freiburg, Germany. jonasp@ruf.uni-freiburg.de〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9665886" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Baclofen/pharmacology ; Bicuculline/pharmacology ; GABA Antagonists ; GABA-A Receptor Antagonists ; GABA-B Receptor Antagonists ; Glycine/*metabolism ; Glycine Agents/pharmacology ; In Vitro Techniques ; Interneurons/drug effects/*metabolism ; Motor Neurons/drug effects/*metabolism ; Patch-Clamp Techniques ; Presynaptic Terminals/*metabolism ; Rats ; Rats, Wistar ; Receptors, GABA-A/metabolism ; Receptors, GABA-B/metabolism ; Receptors, Glycine/antagonists & inhibitors/metabolism ; Spinal Cord/cytology ; Strychnine/pharmacology ; Synaptic Transmission/drug effects ; Synaptic Vesicles/metabolism ; gamma-Aminobutyric Acid/*metabolism
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  • 32
    Publication Date: 1998-02-21
    Description: Syntaxins are thought to function during vesicular transport as receptors on the target membrane and to contribute to the specificity of membrane docking and fusion by interacting with vesicle-associated receptors. Here, syntaxin 5 (Syn5) was shown to be an integral component of endoplasmic reticulum-derived transport vesicles. This pool, but not the target, Golgi-associated Syn5 pool, was essential for the assembly of vesicular-tubular pre-Golgi intermediates and the delivery of cargo to the Golgi. The requirement for vesicle-associated Syn5 in transport suggests a reevaluation of the basis for operation of the early secretory pathway.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rowe, T -- Dascher, C -- Bannykh, S -- Plutner, H -- Balch, W E -- CA58689/CA/NCI NIH HHS/ -- GM 42336/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 30;279(5351):696-700.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biology, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9445473" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Antibodies ; Biological Transport ; Carrier Proteins/metabolism ; Cell Line ; Endoplasmic Reticulum/*metabolism ; Golgi Apparatus/*metabolism/ultrastructure ; Mannose-Binding Lectins ; Membrane Fusion ; *Membrane Glycoproteins ; Membrane Proteins/immunology/*metabolism ; N-Ethylmaleimide-Sensitive Proteins ; Organelles/metabolism ; Qa-SNARE Proteins ; Qb-SNARE Proteins ; Qc-SNARE Proteins ; R-SNARE Proteins ; Rats ; SNARE Proteins ; *Vesicular Transport Proteins ; Vesicular stomatitis Indiana virus/physiology ; Viral Envelope Proteins/metabolism
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  • 33
    Publication Date: 1998-07-10
    Description: A new method for magnetic resonance imaging (MRI) based on the detection of relatively strong signal from intermolecular zero-quantum coherences (iZQCs) is reported. Such a signal would not be observable in the conventional framework of magnetic resonance; it originates in long-range dipolar couplings (10 micrometers to 1 millimeter) that are traditionally ignored. Unlike conventional MRI, where image contrast is based on variations in spin density and relaxation times (often with injected contrast agents), contrast with iZQC images comes from variations in the susceptibility over a distance dictated by gradient strength. Phantom and in vivo (rat brain) data confirm that iZQC images give contrast enhancement. This contrast might be useful in the detection of small tumors, in that susceptibility correlates with oxygen concentration and in functional MRI.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warren, W S -- Ahn, S -- Mescher, M -- Garwood, M -- Ugurbil, K -- Richter, W -- Rizi, R R -- Hopkins, J -- Leigh, J S -- GM35253/GM/NIGMS NIH HHS/ -- RR02305/RR/NCRR NIH HHS/ -- RR08079/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Jul 10;281(5374):247-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Chemistry, Princeton University, Princeton, NJ 08544-1009, USA. wwarren@princeton.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9657717" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*anatomy & histology/physiology ; Brain Mapping ; Brain Neoplasms/*pathology ; Magnetic Resonance Imaging/*methods ; Magnetics ; Mathematics ; Phantoms, Imaging ; Rats
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  • 34
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-07
    Description: The tetrodotoxin-sensitive sodium ion (Na+) channel is opened by cellular depolarization and favors the passage of Na+ over other ions. Activation of the beta-adrenergic receptor or protein kinase A in rat heart cells transformed this Na+ channel into one that is promiscuous with respect to ion selectivity, permitting calcium ions (Ca2+) to permeate as readily as Na+. Similarly, nanomolar concentrations of cardiotonic steroids such as ouabain and digoxin switched the ion selectivity of the Na+ channel to this state of promiscuous permeability called slip-mode conductance. Slip-mode conductance of the Na+ channel can contribute significantly to local and global cardiac Ca2+ signaling and may be a general signaling mechanism in excitable cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Santana, L F -- Gomez, A M -- Lederer, W J -- New York, N.Y. -- Science. 1998 Feb 13;279(5353):1027-33.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, Medical Biotechnology Center and School of Medicine, University of Maryland, 725 West Lombard Street, Baltimore, MD 21201, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9461434" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Calcium/*metabolism ; Cardiotonic Agents/pharmacology ; Cyclic AMP/metabolism ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Digoxin/pharmacology ; Enzyme Activation ; In Vitro Techniques ; Ion Channel Gating ; Isoproterenol/pharmacology ; Myocardial Contraction/*physiology ; Myocardium/cytology/*metabolism ; Ouabain/pharmacology ; Patch-Clamp Techniques ; Rats ; Receptors, Adrenergic, beta/physiology ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/*metabolism ; Signal Transduction ; Sodium/metabolism ; Sodium Channel Blockers ; Sodium Channels/drug effects/*metabolism ; Sodium-Calcium Exchanger/metabolism ; Tetrodotoxin/pharmacology
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  • 35
    Publication Date: 1998-06-25
    Description: Long-term potentiation (LTP) at the Schaffer collateral-CA1 synapse involves interacting signaling components, including calcium (Ca2+)/calmodulin-dependent protein kinase II (CaMKII) and cyclic adenosine monophosphate (cAMP) pathways. Postsynaptic injection of thiophosphorylated inhibitor-1 protein, a specific inhibitor of protein phosphatase-1 (PP1), substituted for cAMP pathway activation in LTP. Stimulation that induced LTP triggered cAMP-dependent phosphorylation of endogenous inhibitor-1 and a decrease in PP1 activity. This stimulation also increased phosphorylation of CaMKII at Thr286 and Ca2+-independent CaMKII activity in a cAMP-dependent manner. The blockade of LTP by a CaMKII inhibitor was not overcome by thiophosphorylated inhibitor-1. Thus, the cAMP pathway uses PP1 to gate CaMKII signaling in LTP.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blitzer, R D -- Connor, J H -- Brown, G P -- Wong, T -- Shenolikar, S -- Iyengar, R -- Landau, E M -- DK52054/DK/NIDDK NIH HHS/ -- GM54508/GM/NIGMS NIH HHS/ -- NS33646/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 19;280(5371):1940-2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Bronx VA Medical Center and Department of Psychiatry, Mount Sinai School of Medicine, New York, NY 10029, USA. rb2@doc.mssm.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9632393" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 ; Calcium-Calmodulin-Dependent Protein Kinases/antagonists & inhibitors/*metabolism ; *Carrier Proteins ; Cyclic AMP/analogs & derivatives/*metabolism/pharmacology ; Cyclic AMP-Dependent Protein Kinases/metabolism ; Electric Stimulation ; Enzyme Inhibitors/metabolism/pharmacology ; Hippocampus/*metabolism ; In Vitro Techniques ; *Intracellular Signaling Peptides and Proteins ; *Long-Term Potentiation ; Male ; Phosphoprotein Phosphatases/antagonists & inhibitors/*metabolism ; Phosphorylation ; Protein Phosphatase 1 ; RNA-Binding Proteins/metabolism/pharmacology ; Rats ; Rats, Sprague-Dawley ; Signal Transduction ; Synapses/*metabolism ; Thionucleotides/pharmacology
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  • 36
    Publication Date: 1998-06-20
    Description: Many of aspirin's therapeutic effects arise from its acetylation of cyclooxygenase-2 (COX-2), whereas its antithrombotic and ulcerogenic effects result from its acetylation of COX-1. Here, aspirin-like molecules were designed that preferentially acetylate and irreversibly inactivate COX-2. The most potent of these compounds was o-(acetoxyphenyl)hept-2-ynyl sulfide (APHS). Relative to aspirin, APHS was 60 times as reactive against COX-2 and 100 times as selective for its inhibition; it also inhibited COX-2 in cultured macrophages and colon cancer cells and in the rat air pouch in vivo. Such compounds may lead to the development of aspirin-like drugs for the treatment or prevention of immunological and proliferative diseases without gastrointestinal or hematologic side effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kalgutkar, A S -- Crews, B C -- Rowlinson, S W -- Garner, C -- Seibert, K -- Marnett, L J -- CA47479/CA/NCI NIH HHS/ -- CA68485/CA/NCI NIH HHS/ -- ES00267/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1998 May 22;280(5367):1268-70.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉A.B. Hancock Jr. Memorial Laboratory for Cancer Research, Vanderbilt Cancer Center, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596581" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylation ; Acetylene/*analogs & derivatives/chemical synthesis/chemistry/pharmacology ; Alkynes ; Animals ; Anti-Inflammatory Agents, Non-Steroidal/*chemical ; synthesis/chemistry/pharmacology ; Aspirin/chemistry/pharmacology ; Binding Sites ; Cell Division/drug effects ; Cell Line ; Colonic Neoplasms/enzymology/pathology ; Cyclooxygenase 2 ; Cyclooxygenase 2 Inhibitors ; Cyclooxygenase Inhibitors/*chemical synthesis/chemistry/pharmacology ; Dinoprostone/biosynthesis ; Drug Design ; Humans ; Indomethacin/pharmacology ; Isoenzymes/chemistry/genetics/*metabolism ; Macrophages/enzymology ; Membrane Proteins ; Mutagenesis, Site-Directed ; Prostaglandin D2/biosynthesis ; Prostaglandin-Endoperoxide Synthases/chemistry/genetics/*metabolism ; Rats ; Rats, Inbred Lew ; Sulfides/*chemical synthesis/chemistry/pharmacology ; Thromboxane B2/biosynthesis ; Tumor Cells, Cultured
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-08-26
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Blusztajn, J K -- New York, N.Y. -- Science. 1998 Aug 7;281(5378):794-5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Boston University School of Medicine, Boston, MA 02118, USA. jbluszta@bu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9714685" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Aging ; Animals ; Apoptosis ; Brain/cytology/*embryology/growth & development/*physiology ; Cell Division ; Choline/*administration & dosage/*metabolism ; Choline Deficiency/physiopathology ; Cognition ; Diet ; Female ; Hippocampus/metabolism ; Humans ; Long-Term Potentiation ; Maternal-Fetal Exchange ; Memory ; Nutrition Policy ; Pregnancy ; Rats
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  • 38
    Publication Date: 1998-06-20
    Description: Stimulation of T lymphocytes results in a rapid increase in intracellular calcium concentration ([Ca2+]i) that parallels the activation of Ca2+-calmodulin-dependent protein kinase IV (CaMKIV), a nuclear enzyme that can phosphorylate and activate the cyclic adenosine monophosphate (cAMP) response element-binding protein (CREB). However, inactivation of CaMKIV occurs despite the sustained increase in [Ca2+]i that is required for T cell activation. A stable and stoichiometric complex of CaMKIV with protein serine-threonine phosphatase 2A (PP2A) was identified in which PP2A dephosphorylates CaMKIV and functions as a negative regulator of CaMKIV signaling. In Jurkat T cells, inhibition of PP2A activity by small t antigen enhanced activation of CREB-mediated transcription by CaMKIV. These findings reveal an intracellular signaling mechanism whereby a protein serine-threonine kinase (CaMKIV) is regulated by a tightly associated protein serine-threonine phosphatase (PP2A).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Westphal, R S -- Anderson, K A -- Means, A R -- Wadzinski, B E -- GM33976/GM/NIGMS NIH HHS/ -- GM51366/GM/NIGMS NIH HHS/ -- HD07503/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 May 22;280(5367):1258-61.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, TN 37232, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9596578" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Polyomavirus Transforming/metabolism ; Brain/enzymology ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 4 ; Calcium-Calmodulin-Dependent Protein Kinases/genetics/isolation & ; purification/*metabolism ; Calmodulin/metabolism ; Coenzymes/metabolism ; Cyclic AMP Response Element-Binding Protein/metabolism ; Enzyme Activation ; Humans ; Jurkat Cells ; Lymphocyte Activation ; Mutation ; Phosphoprotein Phosphatases/isolation & purification/*metabolism ; Phosphorylation ; Protein Phosphatase 2 ; Rats ; Recombinant Fusion Proteins/metabolism ; *Signal Transduction ; T-Lymphocytes/*enzymology ; Transcription, Genetic
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  • 39
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-10-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bliss, T V -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):1975-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neurophysiology, National Institute for Medical Research, London Nw7 1AA, UK. tbliss@ns1.nimr.mrc.ac.uk〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9767047" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/physiology ; Dentate Gyrus/physiology ; Electric Stimulation ; Electrodes, Implanted ; Hippocampus/*physiology ; Long-Term Potentiation/*physiology ; Maze Learning/*physiology ; Perforant Pathway/physiology ; Pyramidal Cells/physiology ; Rats ; Synapses/*physiology ; Tetany
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  • 40
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-05-09
    Description: Fluorescence in situ hybridization (FISH) and digital imaging microscopy were modified to allow detection of single RNA molecules. Oligodeoxynucleotide probes were synthesized with five fluorochromes per molecule, and the light emitted by a single probe was calibrated. Points of light in exhaustively deconvolved images of hybridized cells gave fluorescent intensities and distances between probes consistent with single messenger RNA molecules. Analysis of beta-actin transcription sites after serum induction revealed synchronous and cyclical transcription from single genes. The rates of transcription initiation and termination and messenger RNA processing could be determined by positioning probes along the transcription unit. This approach extends the power of FISH to yield quantitative molecular information on a single cell.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Femino, A M -- Fay, F S -- Fogarty, K -- Singer, R H -- GM 54887/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1998 Apr 24;280(5363):585-90.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology and Cell Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9554849" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/genetics ; Animals ; Cell Line ; Fluorescein-5-isothiocyanate ; *In Situ Hybridization, Fluorescence ; Kinetics ; Oligonucleotide Probes ; RNA Processing, Post-Transcriptional ; RNA, Messenger/*analysis/*genetics/metabolism ; Rats ; *Transcription, Genetic
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  • 41
    Publication Date: 1998-08-28
    Description: Glutamatergic abnormalities have been associated with several psychiatric disorders, including schizophrenia and addiction. Group II metabotropic glutamate receptors were targeted to normalize glutamatergic disruptions associated with an animal model of schizophrenia, the phencyclidine model. An agonist of this group of receptors, at a dose that was without effects on spontaneous activity and corticolimbic dopamine neurotransmission, attenuated the disruptive effects of phencyclidine on working memory, stereotypy, locomotion, and cortical glutamate efflux. This behavioral reversal occurred in spite of sustained dopamine hyperactivity. Thus, targeting this group of receptors may present a nondopaminergic therapeutic strategy for treatment of psychiatric disorders.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moghaddam, B -- Adams, B W -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1349-52.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychiatry, Yale University School of Medicine, Veterans Administration Medical Center 116A/2, West Haven, CT 06516, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9721099" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicyclo Compounds/administration & dosage/*pharmacology/therapeutic use ; Disease Models, Animal ; Dopamine/metabolism ; Excitatory Amino Acid Agonists/administration & dosage/*pharmacology/therapeutic ; use ; Glutamic Acid/metabolism ; Male ; Memory/drug effects ; Motor Activity/drug effects ; Nucleus Accumbens/drug effects/metabolism ; Phencyclidine/*pharmacology ; Prefrontal Cortex/drug effects/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Metabotropic Glutamate/*agonists/metabolism ; Schizophrenia/chemically induced/*drug therapy/metabolism ; Stereotyped Behavior/drug effects ; Synaptic Transmission/drug effects
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  • 42
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-28
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Juliano, S L -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1653-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Cell Biology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, USA. sjuliano@mx3.usuhs.mil〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9518376" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Acoustic Stimulation ; Animals ; Auditory Cortex/*physiology ; Basal Ganglia/*physiology ; *Brain Mapping ; Electric Stimulation ; *Neuronal Plasticity ; Prosencephalon/*physiology ; Rats ; Receptors, Muscarinic/physiology ; Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
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  • 43
    Publication Date: 1998-10-23
    Description: Patients with abetalipoproteinemia, a disease caused by defects in the microsomal triglyceride transfer protein (MTP), do not produce apolipoprotein B-containing lipoproteins. It was hypothesized that small molecule inhibitors of MTP would prevent the assembly and secretion of these atherogenic lipoproteins. To test this hypothesis, two compounds identified in a high-throughput screen for MTP inhibitors were used to direct the synthesis of a highly potent MTP inhibitor. This molecule (compound 9) inhibited the production of lipoprotein particles in rodent models and normalized plasma lipoprotein levels in Watanabe-heritable hyperlipidemic (WHHL) rabbits, which are a model for human homozygous familial hypercholesterolemia. These results suggest that compound 9, or derivatives thereof, has potential applications for the therapeutic lowering of atherogenic lipoprotein levels in humans.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wetterau, J R -- Gregg, R E -- Harrity, T W -- Arbeeny, C -- Cap, M -- Connolly, F -- Chu, C H -- George, R J -- Gordon, D A -- Jamil, H -- Jolibois, K G -- Kunselman, L K -- Lan, S J -- Maccagnan, T J -- Ricci, B -- Yan, M -- Young, D -- Chen, Y -- Fryszman, O M -- Logan, J V -- Musial, C L -- Poss, M A -- Robl, J A -- Simpkins, L M -- Slusarchyk, W A -- Sulsky, R -- Taunk, P -- Magnin, D R -- Tino, J A -- Lawrence, R M -- Dickson, J K Jr -- Biller, S A -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):751-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Metabolic Diseases, Bristol-Myers Squibb Pharmaceutical Research Institute, Princeton, NJ 08543-4000, USA. Wetterau_John_R@msmail.bms.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784135" target="_blank"〉PubMed〈/a〉
    Keywords: Alanine Transaminase/blood ; Animals ; Apolipoproteins B/*blood ; Aspartate Aminotransferases/blood ; Carrier Proteins/*antagonists & inhibitors ; Cholesterol/*blood ; Cricetinae ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Drug Design ; Drug Evaluation, Preclinical ; Fluorenes/chemistry/pharmacokinetics/*pharmacology ; Humans ; Hyperlipidemias/blood/drug therapy ; Hyperlipoproteinemia Type II/*blood/drug therapy ; Lipids/blood ; Lipoproteins/blood ; Liver/metabolism ; Mice ; Piperidines/chemistry/pharmacokinetics/*pharmacology ; Rabbits ; Rats ; Triglycerides/*blood/metabolism ; Tumor Cells, Cultured
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  • 44
    Publication Date: 1998-12-18
    Description: cAMP (3',5' cyclic adenosine monophosphate) is a second messenger that in eukaryotic cells induces physiological responses ranging from growth, differentiation, and gene expression to secretion and neurotransmission. Most of these effects have been attributed to the binding of cAMP to cAMP-dependent protein kinase A (PKA). Here, a family of cAMP-binding proteins that are differentially distributed in the mammalian brain and body organs and that exhibit both cAMP-binding and guanine nucleotide exchange factor (GEF) domains is reported. These cAMP-regulated GEFs (cAMP-GEFs) bind cAMP and selectively activate the Ras superfamily guanine nucleotide binding protein Rap1A in a cAMP-dependent but PKA-independent manner. Our findings suggest the need to reformulate concepts of cAMP-mediated signaling to include direct coupling to Ras superfamily signaling.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kawasaki, H -- Springett, G M -- Mochizuki, N -- Toki, S -- Nakaya, M -- Matsuda, M -- Housman, D E -- Graybiel, A M -- P01 CA42063/CA/NCI NIH HHS/ -- P01 HL41484/HL/NHLBI NIH HHS/ -- R01 HD28341/HD/NICHD NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1998 Dec 18;282(5397):2275-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Brain and Cognitive Sciences, Massachusetts Institute of Technology (MIT), Cambridge, MA, 02139, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9856955" target="_blank"〉PubMed〈/a〉
    Keywords: 1-Methyl-3-isobutylxanthine/pharmacology ; Adrenal Glands/metabolism ; Adult ; Amino Acid Sequence ; Animals ; Brain/metabolism ; Cell Line ; Colforsin/pharmacology ; Cyclic AMP/*metabolism ; Cyclic AMP-Dependent Protein Kinases/antagonists & inhibitors/metabolism ; Fetus/metabolism ; GTP-Binding Proteins/*metabolism ; Gene Expression ; Guanine Nucleotide Exchange Factors ; Humans ; In Situ Hybridization ; Molecular Sequence Data ; Phosphorylation ; Proteins/chemistry/genetics/*metabolism ; Rats ; Second Messenger Systems ; Sequence Deletion ; Signal Transduction ; rap GTP-Binding Proteins ; ras Guanine Nucleotide Exchange Factors
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  • 45
    Publication Date: 1998-12-16
    Description: alpha-Dystroglycan (alpha-DG) is a component of the dystroglycan complex, which is involved in early development and morphogenesis and in the pathogenesis of muscular dystrophies. Here, alpha-DG was shown to serve as a Schwann cell receptor for Mycobacterium leprae, the causative organism of leprosy. Mycobacterium leprae specifically bound to alpha-DG only in the presence of the G domain of the alpha2 chain of laminin-2. Native alpha-DG competitively inhibited the laminin-2-mediated M. leprae binding to primary Schwann cells. Thus, M. leprae may use linkage between the extracellular matrix and cytoskeleton through laminin-2 and alpha-DG for its interaction with Schwann cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rambukkana, A -- Yamada, H -- Zanazzi, G -- Mathus, T -- Salzer, J L -- Yurchenco, P D -- Campbell, K P -- Fischetti, V A -- New York, N.Y. -- Science. 1998 Dec 11;282(5396):2076-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Bacterial Pathogenesis and Immunology, Rockefeller University, New York, NY 10021, USA. rambuka@rockvax.rockefeller.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9851927" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bacterial Adhesion ; Binding Sites ; Calcium/physiology ; Cell Line, Transformed ; Cells, Cultured ; Cytoskeletal Proteins/*metabolism/pharmacology ; Dystroglycans ; Edetic Acid/pharmacology ; Glycosylation ; Humans ; Laminin/chemistry/*metabolism ; Membrane Glycoproteins/*metabolism/pharmacology ; Mycobacterium leprae/*metabolism ; Peripheral Nerves/chemistry ; Rats ; Receptors, Laminin/metabolism ; Recombinant Fusion Proteins/metabolism ; Recombinant Proteins/chemistry/metabolism ; Schwann Cells/metabolism/*microbiology
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  • 46
    Publication Date: 1998-01-24
    Description: Development of analgesic agents for the treatment of severe pain requires the identification of compounds that are devoid of opioid receptor liabilities. A potent (inhibition constant = 37 picomolar) neuronal nicotinic acetylcholine receptor (nAChR) ligand called ABT-594 was developed that has antinociceptive properties equal in efficacy to those of morphine across a series of diverse animal models of acute thermal, persistent chemical, and neuropathic pain states. These effects were blocked by the nAChR antagonist mecamylamine. In contrast to morphine, repeated treatment with ABT-594 did not appear to elicit opioid-like withdrawal or physical dependence. Thus, ABT-594 may be an analgesic that lacks the problems associated with opioid analgesia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bannon, A W -- Decker, M W -- Holladay, M W -- Curzon, P -- Donnelly-Roberts, D -- Puttfarcken, P S -- Bitner, R S -- Diaz, A -- Dickenson, A H -- Porsolt, R D -- Williams, M -- Arneric, S P -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):77-81.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurological and Urological Diseases Research, Pharmaceutical Products Division, Abbott Laboratories, Abbott Park, IL 60064-3500, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417028" target="_blank"〉PubMed〈/a〉
    Keywords: Analgesics, Non-Narcotic/chemical synthesis/metabolism/*pharmacology ; Animals ; Azetidines/chemical synthesis/metabolism/*pharmacology ; Bicyclo Compounds, Heterocyclic/pharmacology ; Capsaicin/pharmacology ; Dose-Response Relationship, Drug ; In Vitro Techniques ; Ligands ; Mecamylamine/pharmacology ; Morphine/pharmacology ; Nerve Fibers/drug effects/metabolism/physiology ; Neuromuscular Junction/metabolism ; Neurons/drug effects/metabolism/physiology ; Nicotine/pharmacology ; Nicotinic Agonists/chemical synthesis/metabolism/*pharmacology ; Nicotinic Antagonists/pharmacology ; Pain/drug therapy ; Pain Measurement ; Pyridines/chemical synthesis/metabolism/*pharmacology ; Rats ; Receptors, Nicotinic/*metabolism ; Spinal Cord/drug effects/metabolism/physiology ; Substance Withdrawal Syndrome/etiology ; Synaptic Transmission/drug effects
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  • 47
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Barinaga, M -- New York, N.Y. -- Science. 1998 Nov 6;282(5391):1018-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841441" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/embryology ; Cell Differentiation ; Clone Cells ; Dentate Gyrus/cytology ; Fetus ; Humans ; Neuroglia/*cytology ; Neurons/*cytology/physiology ; Rats ; Regeneration ; Stem Cell Transplantation ; Stem Cells/*cytology
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  • 48
    Publication Date: 1998-09-25
    Description: The proapoptotic Bax protein induces cell death by acting on mitochondria. Bax binds to the permeability transition pore complex (PTPC), a composite proteaceous channel that is involved in the regulation of mitochondrial membrane permeability. Immunodepletion of Bax from PTPC or purification of PTPC from Bax-deficient mice yielded a PTPC that could not permeabilize membranes in response to atractyloside, a proapoptotic ligand of the adenine nucleotide translocator (ANT). Bax and ANT coimmunoprecipitated and interacted in the yeast two-hybrid system. Ectopic expression of Bax induced cell death in wild-type but not in ANT-deficient yeast. Recombinant Bax and purified ANT, but neither of them alone, efficiently formed atractyloside-responsive channels in artificial membranes. Hence, the proapoptotic molecule Bax and the constitutive mitochondrial protein ANT cooperate within the PTPC to increase mitochondrial membrane permeability and to trigger cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Marzo, I -- Brenner, C -- Zamzami, N -- Jurgensmeier, J M -- Susin, S A -- Vieira, H L -- Prevost, M C -- Xie, Z -- Matsuyama, S -- Reed, J C -- Kroemer, G -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2027-31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CNRS, UPR 420, 19 rue Guy Moquet, F-94801 Villejuif, France.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748162" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Apoptosis ; Atractyloside/metabolism/pharmacology ; Binding Sites ; Bongkrekic Acid/metabolism/pharmacology ; Cyclosporine/pharmacology ; Dimerization ; HT29 Cells ; Humans ; Intracellular Membranes/physiology ; Liposomes ; Mice ; Mice, Inbred C57BL ; Mitochondria/*physiology ; Mitochondrial ADP, ATP Translocases/chemistry/*metabolism ; Permeability ; Proto-Oncogene Proteins/chemistry/genetics/*metabolism/pharmacology ; Proto-Oncogene Proteins c-bcl-2/pharmacology ; Rats ; Rats, Wistar ; Recombinant Proteins/pharmacology ; Saccharomyces cerevisiae/cytology/genetics ; Transfection ; bcl-2-Associated X Protein
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  • 49
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-12-05
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Peters, R -- Sikorski, R -- New York, N.Y. -- Science. 1998 Oct 16;282(5388):432-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9841402" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arteries/*anatomy & histology ; Helium ; Isotopes ; Magnetic Resonance Imaging/*methods ; Rats ; Rats, Sprague-Dawley ; Veins/*anatomy & histology
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  • 50
    Publication Date: 1998-10-23
    Description: Nonpeptide agonists of each of the five somatostatin receptors were identified in combinatorial libraries constructed on the basis of molecular modeling of known peptide agonists. In vitro experiments using these selective compounds demonstrated the role of the somatostatin subtype-2 receptor in inhibition of glucagon release from mouse pancreatic alpha cells and the somatostatin subtype-5 receptor as a mediator of insulin secretion from pancreatic beta cells. Both receptors regulated growth hormone release from the rat anterior pituitary gland. The availability of high-affinity, subtype-selective agonists for each of the somatostatin receptors provides a direct approach to defining their physiological functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rohrer, S P -- Birzin, E T -- Mosley, R T -- Berk, S C -- Hutchins, S M -- Shen, D M -- Xiong, Y -- Hayes, E C -- Parmar, R M -- Foor, F -- Mitra, S W -- Degrado, S J -- Shu, M -- Klopp, J M -- Cai, S J -- Blake, A -- Chan, W W -- Pasternak, A -- Yang, L -- Patchett, A A -- Smith, R G -- Chapman, K T -- Schaeffer, J M -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):737-40.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cell Biochemistry and Physiology, Merck Research Laboratories, Post Office Box 2000, Rahway, NJ 07065, USA. susanvrohrer@merck.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784130" target="_blank"〉PubMed〈/a〉
    Keywords: Amides/metabolism/*pharmacology ; Amino Acid Sequence ; Animals ; Cell Line ; Cells, Cultured ; Cricetinae ; Drug Design ; Glucagon/secretion ; Growth Hormone/secretion ; Insulin/secretion ; Islets of Langerhans/drug effects/secretion ; Ligands ; Membrane Proteins ; Mice ; Models, Chemical ; Molecular Sequence Data ; Pituitary Gland, Anterior/drug effects/metabolism ; Rats ; Receptors, Somatostatin/*agonists/physiology
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  • 51
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-08-15
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Malissen, B -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):528-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie INSERM-CNRS de Marseille-Luminy, Marseille, France. bernardm@ciml.univ-mrs.fr〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9705722" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens/immunology ; Antigens, CD3/*metabolism ; Immunoglobulin E/metabolism ; Ligands ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; Rats ; Receptor Aggregation ; Receptor-CD3 Complex, Antigen, T-Cell/metabolism ; Receptors, Antigen, T-Cell/*metabolism ; Receptors, IgE/*metabolism ; Signal Transduction ; T-Lymphocytes/immunology
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  • 52
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cook-Deegan, R M -- New York, N.Y. -- Science. 1997 Oct 24;278(5338):560-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9381158" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biological Specimen Banks ; *Cloning, Molecular ; Insulin/*genetics ; *Patents as Topic ; Rats
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  • 53
    Publication Date: 1998-06-06
    Description: RasGRP, a guanyl nucleotide-releasing protein for the small guanosine triphosphatase Ras, was characterized. Besides the catalytic domain, RasGRP has an atypical pair of "EF hands" that bind calcium and a diacylglycerol (DAG)-binding domain. RasGRP activated Ras and caused transformation in fibroblasts. A DAG analog caused sustained activation of Ras-Erk signaling and changes in cell morphology. Signaling was associated with partitioning of RasGRP protein into the membrane fraction. Sustained ligand-induced signaling and membrane partitioning were absent when the DAG-binding domain was deleted. RasGRP is expressed in the nervous system, where it may couple changes in DAG and possibly calcium concentrations to Ras activation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ebinu, J O -- Bottorff, D A -- Chan, E Y -- Stang, S L -- Dunn, R J -- Stone, J C -- New York, N.Y. -- Science. 1998 May 15;280(5366):1082-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Alberta, Edmonton, Alberta, Canada T6G 2H7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9582122" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Brain/*metabolism ; Calcium/metabolism ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Catalysis ; Cell Cycle Proteins/genetics/metabolism ; Cell Line ; Cell Membrane/metabolism ; Cell Size ; Cell Transformation, Neoplastic ; Cloning, Molecular ; DNA, Complementary ; DNA-Binding Proteins/*chemistry/genetics/*metabolism ; Diglycerides/metabolism ; Genes, ras ; *Guanine Nucleotide Exchange Factors ; Guanosine Diphosphate/metabolism ; Guanosine Triphosphate/metabolism ; Molecular Sequence Data ; Neurons/metabolism ; Phosphoprotein Phosphatases/genetics/metabolism ; Rats ; Recombinant Fusion Proteins/metabolism ; Signal Transduction ; ras Proteins/*metabolism ; ras-GRF1
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  • 54
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-01-31
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vogel, G -- New York, N.Y. -- Science. 1998 Jan 9;279(5348):174.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9446221" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/genetics ; Alzheimer Disease/*genetics/metabolism ; Amyloid beta-Protein Precursor/analysis/biosynthesis/*genetics ; Animals ; Brain/*metabolism ; Brain Chemistry ; Down Syndrome/genetics/metabolism ; Frameshift Mutation ; Humans ; RNA, Messenger/genetics ; Rabbits ; Rats ; Sequence Deletion ; Ubiquitins/analysis/biosynthesis/*genetics
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  • 55
    Publication Date: 1998-02-07
    Description: Dynamin guanosine triphosphatases support the scission of clathrin-coated vesicles from the plasmalemma during endocytosis. By fluorescence microscopy of cultured rat hepatocytes, a green fluorescent protein-dynamin II fusion protein localized with clathrin-coated vesicles at the Golgi complex. A cell-free assay was utilized to demonstrate the role of dynamin in vesicle formation at the trans-Golgi. Addition of peptide-specific anti-dynamin antibodies to the assay mixture inhibited both constitutive exocytic and clathrin-coated vesicle formation. Immunodepletion of dynamin proteins also inhibited vesicle formation, and budding efficiency was restored upon readdition of purified dynamin. These data suggest that dynamin participates in the formation of distinct transport vesicles from the trans-Golgi network.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jones, S M -- Howell, K E -- Henley, J R -- Cao, H -- McNiven, M A -- P30 CA-46934/CA/NCI NIH HHS/ -- P30 DK-34914/DK/NIDDK NIH HHS/ -- New York, N.Y. -- Science. 1998 Jan 23;279(5350):573-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Basic Research in Digestive Diseases, Mayo Clinic and Foundation, Rochester, MN 55905, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9438853" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Biological Transport ; Cell Membrane/chemistry ; Cells, Cultured ; Clathrin/analysis ; Coated Vesicles/chemistry/*metabolism/ultrastructure ; Cytosol/metabolism ; Dynamins ; GTP Phosphohydrolases/analysis/immunology/*metabolism ; Golgi Apparatus/chemistry/*metabolism ; Green Fluorescent Proteins ; Guanosine 5'-O-(3-Thiotriphosphate)/metabolism ; Liver/ultrastructure ; Luminescent Proteins ; Microscopy, Fluorescence ; Organelles/chemistry/*metabolism/ultrastructure ; Rats ; Recombinant Fusion Proteins/analysis
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  • 56
    Publication Date: 1998-12-04
    Description: Cortical neurons communicate with various cortical and subcortical targets by way of stereotyped axon projections through the white matter. Slice overlay experiments indicate that the initial growth of cortical axons toward the white matter is regulated by a diffusible chemorepulsive signal localized near the marginal zone. Semaphorin III is a major component of this diffusible signal, and cortical neurons transduce this signal by way of the neuropilin-1 receptor. These observations indicate that semaphorin-neuropilin interactions play a critical role in the initial patterning of projections in the developing cortex.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Polleux, F -- Giger, R J -- Ginty, D D -- Kolodkin, A L -- Ghosh, A -- NS35165/NS/NINDS NIH HHS/ -- NS36176/NS/NINDS NIH HHS/ -- NS534814/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Dec 4;282(5395):1904-6.〈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/9836643" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cell Line ; Cerebral Cortex/*cytology/embryology ; Coculture Techniques ; Gene Targeting ; Glycoproteins/genetics/*physiology ; Humans ; Mice ; Nerve Growth Factors/*metabolism ; Nerve Tissue Proteins/*physiology ; Neurons, Efferent/cytology/*physiology ; Neuropilin-1 ; Rats ; Recombinant Proteins/metabolism ; Semaphorin-3A ; Signal Transduction
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  • 57
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-07-24
    Description: The ratio of late to early events stimulated by the mast cell receptor for immunoglobulin E (IgE) correlated with the affinity of a ligand for the receptor-bound IgE. Because excess receptors clustered by a weakly binding ligand could hoard a critical initiating kinase, they prevented the outnumbered clusters engendered by the high-affinity ligands from launching the more complete cascade. A similar mechanism could explain the antagonistic action of some peptides on the activation of T cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Torigoe, C -- Inman, J K -- Metzger, H -- New York, N.Y. -- Science. 1998 Jul 24;281(5376):568-72.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892-1820, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9677201" target="_blank"〉PubMed〈/a〉
    Keywords: 2,4-Dinitrophenol/immunology ; Adaptor Proteins, Signal Transducing ; Animals ; Antibody Affinity ; Antigen-Antibody Reactions ; Calcium-Calmodulin-Dependent Protein Kinases/metabolism ; Dansyl Compounds ; Enzyme Precursors/metabolism ; Focal Adhesion Kinase 2 ; Haptens/*immunology/metabolism ; Immunoglobulin E/immunology/*metabolism ; Intracellular Signaling Peptides and Proteins ; Ligands ; Mast Cells/*immunology ; Mitogen-Activated Protein Kinase 1 ; Oncogene Proteins/metabolism ; Phosphorylation ; Phosphotyrosine/metabolism ; Protein-Tyrosine Kinases/metabolism ; Rats ; Receptor Aggregation ; Receptors, IgE/immunology/*metabolism ; Signal Transduction ; T-Lymphocytes/immunology ; Tumor Cells, Cultured
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  • 58
    Publication Date: 1998-01-24
    Description: Developing axons reach their final targets as a result of a series of axonal projections to successive intermediate targets. Long-range chemoattraction by intermediate targets plays a key role in this process. Growing axons, however, do not stall at the intermediate targets, where the chemoattractant concentration is expected to be maximal. Commissural axons in the metencephalon, initially attracted by a chemoattractant released from the floor plate, were shown to lose responsiveness to the chemoattractant when they crossed the floor plate in vitro. Such changes in axon responsiveness to chemoattractants may enable developing axons to continue to navigate toward their final destinations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shirasaki, R -- Katsumata, R -- Murakami, F -- New York, N.Y. -- Science. 1998 Jan 2;279(5347):105-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Neuroscience, Division of Biophysical Engineering, Graduate School of Engineering Science, Osaka University, Toyonaka, Osaka 560, Japan. sirasaki@bpe.es.osaka-u.ac.jp〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9417018" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Carbocyanines ; *Cell Adhesion Molecules, Neuronal ; *Chemotaxis ; Contactin 2 ; Culture Techniques ; Fluorescent Dyes ; Membrane Glycoproteins/analysis ; Nerve Growth Factors/*physiology ; Pons/*embryology/physiology ; Rats ; Rats, Wistar ; Rhombencephalon/*embryology/metabolism ; Tumor Suppressor Proteins
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  • 59
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-09-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1998 Aug 28;281(5381):1264-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9735037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bicyclo Compounds/pharmacology/*therapeutic use ; Dopamine/metabolism ; Excitatory Amino Acid Agonists/pharmacology/*therapeutic use ; Glutamic Acid/*metabolism ; Humans ; Maze Learning/drug effects ; Memory/drug effects ; Phencyclidine/pharmacology ; Prefrontal Cortex/drug effects/*metabolism ; Rats ; Receptors, Metabotropic Glutamate/metabolism ; Schizophrenia/chemically induced/*drug therapy/metabolism
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  • 60
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-07-21
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wickelgren, I -- New York, N.Y. -- Science. 1998 Jun 26;280(5372):2045-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9669958" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Deterrents/therapeutic use ; Alcoholism/drug therapy ; Animals ; Behavior, Addictive/drug therapy/*etiology ; Brain/*metabolism ; Cocaine/administration & dosage ; Cocaine-Related Disorders/drug therapy/*etiology ; Excitatory Amino Acid Antagonists/therapeutic use ; Glutamic Acid/*physiology ; Humans ; Rats ; Receptors, Glutamate/metabolism ; Substance-Related Disorders/drug therapy/*etiology ; Synaptic Transmission ; Taurine/analogs & derivatives/therapeutic use
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  • 61
    Publication Date: 1998-06-26
    Description: Hippocampal pyramidal cells are called place cells because each cell tends to fire only when the animal is in a particular part of the environment-the cell's firing field. Acute pharmacological blockade of N-methyl-D-aspartate (NMDA) glutamate receptors was used to investigate how NMDA-based synaptic plasticity participates in the formation and maintenance of the firing fields. The results suggest that the formation and short-term stability of firing fields in a new environment involve plasticity that is independent of NMDA receptor activation. By contrast, the long-term stabilization of newly established firing fields required normal NMDA receptor function and, therefore, may be related to other NMDA-dependent processes such as long-term potentiation and spatial learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kentros, C -- Hargreaves, E -- Hawkins, R D -- Kandel, E R -- Shapiro, M -- Muller, R V -- R01 20686/PHS HHS/ -- R01 45923/PHS HHS/ -- T32 AGO 00189/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1998 Jun 26;280(5372):2121-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Physiology, SUNY Health Science Center Brooklyn, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9641919" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Evoked Potentials ; Excitatory Amino Acid Antagonists/pharmacology ; Hippocampus/*physiology ; Long-Term Potentiation/*physiology ; Male ; Memory/*physiology ; Neuronal Plasticity ; Piperazines/pharmacology ; Pyramidal Cells/*physiology ; Rats ; Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors/*physiology ; Space Perception/*physiology ; Time Factors
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  • 62
    Publication Date: 1998-09-25
    Description: If information is stored as activity-driven increases in synaptic weights in the hippocampal formation, saturation of hippocampal long-term potentiation (LTP) should impair learning. Here, rats in which one hippocampus had been lesioned were implanted with a multielectrode stimulating array across and into the angular bundle afferent to the other hippocampus. Repeated cross-bundle tetanization caused cumulative potentiation. Residual synaptic plasticity was assessed by tetanizing a naive test electrode in the center of the bundle. Spatial learning was disrupted in animals with no residual LTP (〈10 percent) but not in animals that were capable of further potentiation. Thus, saturation of hippocampal LTP impairs spatial learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Moser, E I -- Krobert, K A -- Moser, M B -- Morris, R G -- New York, N.Y. -- Science. 1998 Sep 25;281(5385):2038-42.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Psychology, Norwegian University of Science and Technology, 7034 Trondheim, Norway.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9748165" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dentate Gyrus/physiology ; Electric Stimulation ; Electrodes, Implanted ; Evoked Potentials ; Excitatory Postsynaptic Potentials ; Hippocampus/*physiology ; Long-Term Potentiation/*physiology ; Male ; Maze Learning/*physiology ; Perforant Pathway ; Rats ; Synapses/physiology ; Tetany
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  • 63
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1998-03-28
    Description: Little is known about the mechanisms that allow the cortex to selectively improve the neural representations of behaviorally important stimuli while ignoring irrelevant stimuli. Diffuse neuromodulatory systems may facilitate cortical plasticity by acting as teachers to mark important stimuli. This study demonstrates that episodic electrical stimulation of the nucleus basalis, paired with an auditory stimulus, results in a massive progressive reorganization of the primary auditory cortex in the adult rat. Receptive field sizes can be narrowed, broadened, or left unaltered depending on specific parameters of the acoustic stimulus paired with nucleus basalis activation. This differential plasticity parallels the receptive field remodeling that results from different types of behavioral training. This result suggests that input characteristics may be able to drive appropriate alterations of receptive fields independently of explicit knowledge of the task. These findings also suggest that the basal forebrain plays an active instructional role in representational plasticity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kilgard, M P -- Merzenich, M M -- NS-10414/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1998 Mar 13;279(5357):1714-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Otolaryngology, W. M. Keck Foundation Center for Integrative Neuroscience, University of California, San Francisco, 513 Parnassus Avenue, Box 0732, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9497289" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Acoustic Stimulation ; Animals ; Auditory Cortex/*physiology ; Basal Ganglia/*physiology ; *Brain Mapping ; Conditioning (Psychology) ; Electric Stimulation ; *Neuronal Plasticity ; Neurons/physiology ; Prosencephalon/*physiology ; Rats
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  • 64
    Publication Date: 1998-10-23
    Description: A map of 30,181 human gene-based markers was assembled and integrated with the current genetic map by radiation hybrid mapping. The new gene map contains nearly twice as many genes as the previous release, includes most genes that encode proteins of known function, and is twofold to threefold more accurate than the previous version. A redesigned, more informative and functional World Wide Web site (www.ncbi.nlm.nih.gov/genemap) provides the mapping information and associated data and annotations. This resource constitutes an important infrastructure and tool for the study of complex genetic traits, the positional cloning of disease genes, the cross-referencing of mammalian genomes, and validated human transcribed sequences for large-scale studies of gene expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deloukas, P -- Schuler, G D -- Gyapay, G -- Beasley, E M -- Soderlund, C -- Rodriguez-Tome, P -- Hui, L -- Matise, T C -- McKusick, K B -- Beckmann, J S -- Bentolila, S -- Bihoreau, M -- Birren, B B -- Browne, J -- Butler, A -- Castle, A B -- Chiannilkulchai, N -- Clee, C -- Day, P J -- Dehejia, A -- Dibling, T -- Drouot, N -- Duprat, S -- Fizames, C -- Fox, S -- Gelling, S -- Green, L -- Harrison, P -- Hocking, R -- Holloway, E -- Hunt, S -- Keil, S -- Lijnzaad, P -- Louis-Dit-Sully, C -- Ma, J -- Mendis, A -- Miller, J -- Morissette, J -- Muselet, D -- Nusbaum, H C -- Peck, A -- Rozen, S -- Simon, D -- Slonim, D K -- Staples, R -- Stein, L D -- Stewart, E A -- Suchard, M A -- Thangarajah, T -- Vega-Czarny, N -- Webber, C -- Wu, X -- Hudson, J -- Auffray, C -- Nomura, N -- Sikela, J M -- Polymeropoulos, M H -- James, M R -- Lander, E S -- Hudson, T J -- Myers, R M -- Cox, D R -- Weissenbach, J -- Boguski, M S -- Bentley, D R -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 1998 Oct 23;282(5389):744-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Sanger Centre, Hinxton Hall, Hinxton, Cambridge CB10 1SA UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/9784132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chromosomes, Human/*genetics ; Expressed Sequence Tags ; Gene Expression ; Genetic Markers ; *Genome, Human ; Human Genome Project ; Humans ; Internet ; *Physical Chromosome Mapping ; Rats ; Sequence Tagged Sites
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  • 65
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-09-09
    Description: Intracellular recordings from mammalian neuroendocrine cells showed that steady, injected currents can modify and block periodic spike bursts previously associated with increased neurohormone release. Spike afterpotentials could sum to form plateau potentials, which generated bursts and did not depend on axonal conduction or chemical synapses. Therefore, bursting involves a spike-dependent, positive-feedback mechanism endogenous to single neuroendocrine cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Andrew, R D -- Dudek, F E -- NS 16877/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1050-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879204" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; *Electrophysiology ; Evoked Potentials ; Feedback ; Hypothalamus/cytology ; In Vitro Techniques ; Membrane Potentials ; Neurosecretory Systems/cytology/*physiology ; Rats ; Tetrodotoxin/pharmacology
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  • 66
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-03-25
    Description: The activity of 7,12-dimethylbenz[a]anthracene hydroxylase in the rat ovary is several times higher in the proestrous phase of the estrous cycle than in the estrous and metestrous plus diestrous phases. Administration of gonadotropin leads to a similar increase in the capacity of the ovary to metabolize xenobiotics. This variation in the activity of 7,12-dimethylbenz[a]anthracene hydroxylase during the estrous cycle may be related to the marked changes in the incidence of ovarian cancer during menopause and in women taking contraceptive pills.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bengtsson, M -- Rydstrom, J -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1437-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6681915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aryl Hydrocarbon Hydroxylases/*metabolism ; Cytochrome P-450 Enzyme System/metabolism ; Epoxide Hydrolases/metabolism ; *Estrus ; Female ; Glutathione Transferase/metabolism ; Gonadotropins, Equine/*pharmacology ; Metestrus ; Ovary/*physiology ; Pregnancy ; Proestrus ; Quinone Reductases/metabolism ; Rats ; Rats, Inbred Strains
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  • 67
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-12-16
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉New York, N.Y. -- Science. 1983 Dec 16;222(4629):1251-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6648532" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/drug effects ; Flupenthixol/*pharmacology ; Hypothalamus/*drug effects ; Kinetics ; Rats ; *Reward ; Self Stimulation/*drug effects ; Thioxanthenes/*pharmacology
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  • 68
    Publication Date: 1983-06-17
    Description: Animals with a history of receiving daily injections of +-amphetamine in a specific environment showed a placebo effect (enhanced activity) when injected with saline and placed there; control animals with similar but dissociated drug histories and experience with the test chamber failed to show the effect. The dopamine receptor blocker pimozide antagonized the establishment of conditioning. However, the same dose of pimozide, when given to previously conditioned animals on the placebo test day, failed to antagonize the expression of conditioned activity. Thus, during conditioning dopaminergic neurons mediated a change that subsequently influenced behavior even when dopaminergic systems were blocked. Although schizophrenia may be related to hyperfunctioning of dopamine, neuroleptic drugs, which block dopamine receptors on their first administration, do not have therapeutic effects for a number of days. The results of the pimozide experiments may resolve this paradox.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beninger, R J -- Hahn, B L -- New York, N.Y. -- Science. 1983 Jun 17;220(4603):1304-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology)/*drug effects/physiology ; Dextroamphetamine/antagonists & inhibitors/*pharmacology ; Humans ; Male ; Pimozide/*pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/physiology ; Reinforcement (Psychology) ; Schizophrenia/physiopathology
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  • 69
    Publication Date: 1983-08-19
    Description: Oral administration of 13-cis-retinoic acid (40 or 160 milligrams per kilogram of body weight daily) significantly reduced the inflammation associated with developing and established adjuvant arthritis, an experimentally induced arthritis in rats that resembles human rheumatoid arthritis. The amount of collagenase secreted in tissue culture by adherent cells isolated from the inflamed joints of adjuvant rats treated with 13-cis-retinoic acid also decreased as compared to the amount secreted by cells from vehicle-treated adjuvant rats. Collagenase is important in the joint destruction accompanying rheumatoid arthritis. The successful use of retinoids in the treatment of this proliferative but nonmalignant disorder demonstrates a new application of these compounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brinckerhoff, C E -- Coffey, J W -- Sullivan, A C -- AM14780/AM/NIADDK NIH HHS/ -- P60 AM20641/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 19;221(4612):756-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6308759" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*drug therapy ; Arthritis, Experimental/*drug therapy ; Female ; Fibrinogen/blood ; Inflammation/drug therapy ; Male ; Microbial Collagenase/biosynthesis ; Prostaglandins E/biosynthesis ; Rats ; Sex Factors ; Tretinoin/*therapeutic use
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  • 70
    Publication Date: 1983-08-12
    Description: Of 76 cutaneously activated neurons recorded from the ventral posterior thalamus of awake, behaving monkeys, nine were weakly excited by innocuous skin stimulation and responded maximally only when noxious mechanical cutaneous stimuli were delivered within small, contralateral receptive fields. These results show that neurons capable of encoding the spatial and temporal features of noxious stimuli are located in the ventral posterior thalamus of the awake primate.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Casey, K L -- Morrow, T J -- NS 12581/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):675-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867738" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cats ; Consciousness/physiology ; Electric Stimulation ; Neurons, Afferent/physiology ; Pain/*physiopathology ; Physical Stimulation ; Rats ; Saimiri ; Thalamic Nuclei/physiology ; Thalamus/cytology/*physiology
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  • 71
    Publication Date: 1983-03-25
    Description: Extracellular single-unit recording techniques were used to test the ability of proglumide to block cholecystokinin-induced excitation of rat midbrain dopaminergic neurons and dopamine-sensitive prefrontal cortex cells. Intravenous and iontophoretic proglumide administration consistently blocked cholecystokinin-induced excitations while having no effect on glutamic acid-induced increases in activity. This selective blockade of central cholecystokinin effects by proglumide suggests that this drug may be valuable for studying the possible role of cholecystokinin as a neurotransmitter or neuromodulator in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chiodo, L A -- Bunney, B S -- MH-25642/MH/NIMH NIH HHS/ -- MH-28849/MH/NIMH NIH HHS/ -- NS-07136/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1449-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828873" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; Cerebral Cortex/physiology ; Cholecystokinin/*pharmacology ; Drug Antagonism ; Glutamine/*analogs & derivatives ; Male ; Mesencephalon/physiology ; Neurons/drug effects/*physiology ; Proglumide/*pharmacology ; Rats
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  • 72
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-11-18
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, J L -- New York, N.Y. -- Science. 1983 Nov 18;222(4625):828-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6138857" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*physiology ; DNA, Recombinant ; Gene Expression Regulation ; Nerve Tissue Proteins/*genetics ; Neurotransmitter Agents/*physiology ; Rats
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  • 73
    Publication Date: 1983-04-29
    Description: Brief deprivation of vision after unilateral lesions of the frontal eye field prevents the appearance of contralateral inattention to visual, auditory, and somatosensory stimuli. The forced circling that accompanies inattention, however, is not affected. An equivalent preoperative period in the dark only partly reduces inattention symptoms. Visual deprivation does not reduce or prevent inattention resulting from lesions of the superior colliculus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Crowne, D P -- Richardson, C M -- Ward, G -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):527-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836298" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Attention/*physiology ; Darkness ; Frontal Lobe/*physiology ; Male ; Movement ; Rats ; Sensory Deprivation/*physiology ; Superior Colliculi/*physiology ; Visual Perception/*physiology
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  • 74
    Publication Date: 1983-07-01
    Description: Mammalian atrial extracts possess natriuretic and diuretic activity. In experiments reported here it was found that atrial, but not ventricular, extract also causes relaxation of isolated vascular and nonvascular smooth muscle preparations. The smooth muscle relaxant activity of atrial extract was heat-stable and concentration-dependent and could be destroyed with protease. Rabbit aortic and chick rectum strips were used for the detection of atrial biological activity. The atrial activity was separated by column chromatography into two peaks having apparent molecular weights of 20,000 to 30,000 and less than 10,000. The atrial substance that copurified with the smooth muscle relaxant activity in both peaks caused natriuresis when injected into conscious rats. It appears that atria possess at least two peptides that elicit smooth muscle relaxation and natriuresis, suggesting an endogenous system of fluid volume regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Currie, M G -- Geller, D M -- Cole, B R -- Boylan, J G -- YuSheng, W -- Holmberg, S W -- Needleman, P -- New York, N.Y. -- Science. 1983 Jul 1;221(4605):71-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857267" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Atrial Function ; Chickens ; Chromatography, Gel ; Dogs ; Dose-Response Relationship, Drug ; Humans ; Molecular Weight ; Muscle, Smooth/drug effects ; Muscle, Smooth, Vascular/*drug effects ; Natriuresis/drug effects ; Rabbits ; Rats ; Swine ; Vasodilation/drug effects
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  • 75
    Publication Date: 1983-07-08
    Description: A diffusible factor produced and secreted by malignant murine cells was capable of inducing plasminogen activator production by normal diploid human fibroblasts. The factor's ability to induce plasminogen activator was insensitive to treatment with nucleases, but its activity was destroyed by digestion with proteases. It is proposed that such a factor would play a role in malignancy if it would recruit normal cells that were adjacent to transformed cells to produce plasminogen activator which could result in tumor-promoted proteolysis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Davies, R L -- Rifkin, D B -- Tepper, R -- Miller, A -- Kucherlapati, R -- CA-16239/CA/NCI NIH HHS/ -- CA-35171/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):171-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6682999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cricetinae ; Fibroblasts/drug effects/metabolism ; Humans ; Hybrid Cells/metabolism ; Melanoma/metabolism ; Mice ; Neoplasms, Experimental/*metabolism/secretion ; Peptides/pharmacology/*secretion ; Plasminogen Activators/*biosynthesis ; Rats
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  • 76
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-07-22
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dermer, G B -- New York, N.Y. -- Science. 1983 Jul 22;221(4608):318.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867709" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Humans ; *Neoplasms ; Neoplasms, Experimental ; Rats ; Research
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  • 77
    Publication Date: 1983-03-18
    Description: Immunohistochemical techniques were used to confirm biochemical evidence that parenchymal cells isolated from adult rat liver and maintained in nonreplicating monolayer culture for 2 days synthesized type IV basement membrane collagen. On continued incubation in serum-free medium, the hepatocytes also synthesized the interstitial collagens, types I and III. Consistent with these results in culture, type IV collagen was localized to the hepatocytes in slices of pathologic rat liver. Hence collagen formation is a previously unrecognized function of the hepatocyte that may be important in the pathogenesis of liver fibrosis or cirrhosis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diegelmann, R F -- Guzelian, P S -- Gay, R -- Gay, S -- AM18976/AM/NIADDK NIH HHS/ -- DE02570/DE/NIDCR NIH HHS/ -- HL11310/HL/NHLBI NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Mar 18;219(4590):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828863" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/metabolism ; Cells, Cultured ; Collagen/*biosynthesis/immunology ; Liver/cytology/*metabolism ; Molecular Weight ; Rats
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  • 78
    Publication Date: 1983-07-08
    Description: Microvoltammetric electrodes were used to monitor dopamine released in the caudate nucleus of the rat after electrical stimulation of the medial forebrain bundle. The time resolution of the technique is sufficient to determine in vivo concentration changes on a time scale of seconds. Direct evidence identifying the substance released as dopamine was obtained both voltammetrically and pharmacologically. Administration of alpha-methyl-p-tyrosine terminates the release of dopamine, although tissue stores of dopamine are still present. Thus there appears to be a compartment for dopamine storage that is not available for immediate release. This compartment appears to be mobilized by amfonelic acid, since administration of this agent after alpha-methyl-p-tyrosine returns the concentration of dopamine released by electrical stimulation to 75 percent of the original amount.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewing, A G -- Bigelow, J C -- Wightman, R M -- KO 4 NS000356/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):169-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857277" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/pharmacology ; Animals ; Caudate Nucleus/drug effects/*metabolism ; Dopamine/*metabolism ; Male ; Methyltyrosines/pharmacology ; Microelectrodes ; Naphthyridines/pharmacology ; Rats ; Rats, Inbred Strains ; alpha-Methyltyrosine
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  • 79
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, J L -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):625-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6603019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Laboratory ; Jurisprudence ; Mice ; *Mice, Inbred BALB C ; Rats ; Rats, Inbred Lew ; Rats, Inbred Strains ; Research ; United States ; Wisconsin
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  • 80
    Publication Date: 1983-02-18
    Description: Cerebral glucose metabolism in rats was examined 1 week after the production by ibotenic acid of unilateral striatal lesions. The incorporation of carbon-14-labeled deoxyglucose decreased within the lesion but much less than that of carbon-14-labeled glucose. Barbiturate anesthesia caused a reversal of the asymmetric striatal deoxyglucose labeling, such that the lesioned striatum retained more tracer than the contralateral side. The combined use of barbiturates and radiolabeled deoxyglucose may enhance the identification of recent brain infarction in experimental animals and in man.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Frey, K A -- Agranoff, B W -- 1 T32 GM07863/GM/NIGMS NIH HHS/ -- NS 15655/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Feb 18;219(4586):879-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6823556" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Barbiturates/*pharmacology ; Brain/*drug effects/metabolism ; Brain Diseases/chemically induced/metabolism ; Corpus Striatum/drug effects ; Deoxyglucose ; Glucose/metabolism ; Ibotenic Acid ; Rats
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  • 81
    Publication Date: 1983-07-29
    Description: Markedly elevated nighttime concentrations of serotonin in rhesus monkey cerebrospinal fluid were reduced to daytime levels by exposing the monkeys to continuous light or to the beta-adrenergic antagonist propranolol. Nighttime elevations of melatonin in cerebrospinal fluid were also suppressed by propranolol and light. Serotonin released in large quantities at night appears to be regulated like melatonin, and may act as a cerebroventricular hormone to influence brain and pituitary function at night.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Garrick, N A -- Tamarkin, L -- Taylor, P L -- Markey, S P -- Murphy, D L -- New York, N.Y. -- Science. 1983 Jul 29;221(4609):474-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6683428" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Circadian Rhythm/drug effects ; Humans ; *Light ; Macaca mulatta ; Male ; Melatonin/physiology ; Propranolol/*pharmacology ; Rats ; Serotonin/*cerebrospinal fluid/physiology
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  • 82
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-05-27
    Description: Postmitochondrial supernatant from rat liver and kidney homogenates transformed cysteine into a mutagen that reverted bacteria of the strain Salmonella typhimurium TA100 to histidine independence. Glutathione was also activated by kidney postmitochondrial supernatant but not by liver preparations. Hence, important endogenous compounds of mammals are positive in the most commonly used short-term test for carcinogenicity and mutagenicity. Glutathione is positive in the test even at concentrations found in mammalian tissues.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glatt, H -- Protic-SabljiC, M -- Oesch, F -- New York, N.Y. -- Science. 1983 May 27;220(4600):961-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6342137" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cysteine/*pharmacology ; Glutathione/*pharmacology ; Histidine/metabolism ; Hydrogen Peroxide/metabolism ; Kidney/metabolism ; Liver/metabolism ; *Mutagenicity Tests ; Mutagens/*pharmacology ; Rats ; Salmonella typhimurium/metabolism
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  • 83
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-08-19
    Description: Neuronal systems involved in the initiation of cocaine reinforcement were investigated by identifying brain sites where direct application of the drug was reinforcing. This was accomplished by allowing rats to self-administer picomolar concentrations of cocaine into discrete brain regions. The medial prefrontal cortex supported self-administration, while the nucleus accumbens and ventral tegmental area did not. Self-administration could be attenuated by including equimolar concentrations of the dopaminergic D2-receptor antagonist sulpiride in the microinjection system. These results imply that cocaine reinforcement is mediated in part through a direct action on mesocortical dopaminergic receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goeders, N E -- Smith, J E -- DA-01999-04/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 19;221(4612):773-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879176" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Mapping ; Cerebral Cortex/*drug effects/physiology ; Cocaine/*pharmacology ; Dopamine/*physiology ; Male ; Nucleus Accumbens/physiology ; Rats ; Self Administration ; Sulpiride/pharmacology
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  • 84
    Publication Date: 1983-08-19
    Description: Cocaine elicited dose-related rotation (circling) in naive rats. The maximum effect was greater than observed previously with other drugs. Overall, females were more sensitive to cocaine than males. However, right-biased females were more sensitive than left-biased females, whereas left-biased males were more sensitive than right-biased males. The results suggest that sex-dependent differences in brain asymmetry may be an important determinant of cocaine sensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Glick, S D -- Hinds, P A -- Shapiro, R M -- DA 01044/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 19;221(4612):775-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6879177" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cocaine/*pharmacology ; Dextroamphetamine/pharmacology ; Female ; Functional Laterality ; Male ; Movement/*drug effects ; Rats ; Rotation ; Sex Factors
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  • 85
    Publication Date: 1983-05-27
    Description: Adenosine receptors were made visible on light microscopy by autoradiography with tritiated cyclohexyladenosine. In the cerebellum, adenosine receptors were absent in Weaver mice, which lack granule cells, and were displaced in Reeler mice, which have displacements of granule cells. Thus, adenosine receptors appear to be located on the axon terminals of excitatory granule cells in the cerebellum. Removal of one eye of a rat depleted adenosine receptors in the contralateral superior colliculus, suggesting that the receptors occur on axon terminals of excitatory projections from retinal ganglion cells. The presence of adenosine receptors on excitatory axon terminals may explain synaptic inhibition by adenosine and the behavioral effects of xanthines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, R R -- Kuhar, M J -- Hester, L -- Snyder, S H -- DA-00266/DA/NIDA NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- NS-16375/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 May 27;220(4600):967-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302841" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Autoradiography ; Axons/*physiology ; Cerebellum/physiology ; Corpus Striatum/physiology ; Hippocampus/physiology ; Mice ; Mice, Neurologic Mutants ; Rats ; Rats, Inbred Strains ; Receptors, Cell Surface/*physiology ; Receptors, Purinergic ; Retinal Ganglion Cells/physiology ; Synaptic Membranes/physiology ; Thalamus/physiology
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  • 86
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-02-04
    Description: The number of transcripts of the cellular oncogene ras, which is homologous to the transforming gene of Harvey sarcoma virus, increases during liver regeneration in rats. The increase in these transcripts in liver polysomal polyadenylated RNA occurs at the time of activation of DNA synthesis during the regenerative process induced by partial hepatectomy or carbon tetrachloride injury. The number of ras transcripts returns to basal levels within 72 hours. These observations show that transcription of a cellular oncogene increases in a regulated way in a nonneoplastic growth process.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goyette, M -- Petropoulos, C J -- Shank, P R -- Fausto, N -- New York, N.Y. -- Science. 1983 Feb 4;219(4584):510-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6297003" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carbon Tetrachloride Poisoning ; DNA/biosynthesis ; Hepatectomy ; *Liver Regeneration ; Nucleic Acid Hybridization ; *Oncogenes ; RNA, Messenger/biosynthesis ; Rats ; Sarcoma Viruses, Murine/genetics ; Time Factors ; *Transcription, Genetic
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  • 87
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-09-16
    Description: In vitro binding studies have demonstrated the existence of multiple opiate receptor types. An additional site in the rat brain (termed the lambda site) is distinct from the established types by its selectivity for 4,5-epoxymorphinans (such as naloxone and morphine). While the lambda site displays a high affinity for naloxone in vivo and in vitro in fresh brain membrane homogenates, these sites rapidly convert in vitro to a state of low affinity. The regional distribution of the lambda site in the brain is strikingly different from that of the classic opiate receptor types.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Grevel, J -- Sadee, W -- AG 031047/AG/NIA NIH HHS/ -- DA 01095/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 16;221(4616):1198-201.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6310750" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Brain Chemistry ; Dihydromorphine/metabolism ; Diprenorphine/metabolism ; Morphine/metabolism ; Nalorphine/metabolism ; Naloxone/*metabolism ; Naltrexone/metabolism ; Rats ; Receptors, Opioid/*metabolism ; Sodium/metabolism ; Tissue Distribution
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  • 88
    Publication Date: 1983-03-25
    Description: Microinfusions of rat prolactin into the dorsal midbrain of estrogen-treated, ovariectomized rats increased lordosis behavior. Midbrain microinfusions of antiserum to prolactin into rats displaying maximum lordosis had the opposite effect. The distribution of a prolactin-like substance in the brain was studied immunocytochemically. The results suggest that a hypothalamic neuronal system projecting to the midbrain contains a prolactin-like substance that plays a role in facilitating this behavior and therefore may mediate some of the effects of estrogen on the brain. These data, together with others from studies of the prolactin gene and its regulation, indicate that it may be possible to analyze a sequence of molecular events in the brain that facilitate a behavioral response.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Harlan, R E -- Shivers, B D -- Pfaff, D W -- HD-05585/HD/NICHD NIH HHS/ -- HD-05737/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1451-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828874" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Castration ; Cerebral Cortex/drug effects/*physiology ; Cosyntropin/pharmacology ; Estradiol/pharmacology ; Female ; Growth Hormone/pharmacology ; Immune Sera ; Kinetics ; Mesencephalon/*physiology ; Oxytocin/pharmacology ; Posture ; Prolactin/administration & dosage/*pharmacology ; Rats ; Sexual Behavior, Animal/*drug effects ; Vasopressins/pharmacology
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  • 89
    Publication Date: 1983-04-15
    Description: Mice infected with reovirus type 1 develop an autoimmune polyendocrine disease. Spleen cells from these mice were fused with myeloma cells and the culture fluids were screened by indirect immunofluorescence for autoantibodies reactive with normal mouse tissues. A large panel of cloned, stable antibody-producing hybridomas has been obtained. Fourteen of the hybridomas make autoantibodies that react with cells in the islets of Langerhans, 24 with cells in the anterior pituitary, 11 with cells in gastric mucosa, and 5 with nuclei. Except for the antibodies to nuclei, the monoclonal autoantibodies are organ-specific. Some, however, show broad cross-species reactivity, recognizing similar antigenic determinants in mouse, rat, pig, and human organs, whereas other recognize determinants only in rodent tissues. Several of the antigens recognized by these monoclonal autoantibodies have been identified as hormones (for example, glucagon, growth hormone, and insulin).〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haspel, M V -- Onodera, T -- Prabhakar, B S -- Horita, M -- Suzuki, H -- Notkins, A L -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):304-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301002" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antibodies, Monoclonal/*immunology ; Autoantibodies/immunology ; Autoimmune Diseases/immunology/*microbiology ; Endocrine Glands/*immunology ; Enzyme-Linked Immunosorbent Assay ; Growth Hormone/immunology ; Humans ; Hybridomas/immunology ; Mice ; Pituitary Gland, Anterior/immunology ; Rats ; Reoviridae Infections/*immunology
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  • 90
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-04-22
    Description: Female mice that had been situated in utero between two female fetuses displayed higher levels of active avoidance responding in adult life than females that had been located between two male fetuses and males for whom uterine position was without effect. Uterine position, therefore, influences acquired as well as species-typical behaviors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hauser, H -- Gandelman, R -- New York, N.Y. -- Science. 1983 Apr 22;220(4595):437-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836288" target="_blank"〉PubMed〈/a〉
    Keywords: Androgens/physiology ; Animals ; Avoidance Learning/*physiology ; Female ; Fetus/*physiology ; Male ; Mice ; Pregnancy ; Rats ; Sex Factors ; Uterus
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  • 91
    Publication Date: 1983-06-10
    Description: A phosphorus-31 nuclear magnetic resonance imaging technique has been used to obtain information on phosphorus metabolites from different spatial regions of tissues in vivo. The technique for selection of planes through the tissue is based on phase-encoding of spin echoes and was used to obtain one-dimensional discrimination of phosphorus-31 spectra from different parts of the tissue simultaneously. Specimens were resolved into 16 distinct slices and a signal-to-noise ratio of about 20 to 1 was obtained in 1/2 hour. Results are presented for phantoms, rat legs, and gerbil heads.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Haselgrove, J C -- Subramanian, V H -- Leigh, J S Jr -- Gyulai, L -- Chance, B -- New York, N.Y. -- Science. 1983 Jun 10;220(4602):1170-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857240" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphate/metabolism ; Animals ; Gerbillinae ; Magnetic Resonance Spectroscopy/*methods ; Phosphocreatine/metabolism ; Phosphoric Acids/metabolism ; Phosphorus/*metabolism ; Rats
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  • 92
    Publication Date: 1983-04-29
    Description: Long-term treatment of rats with atropine induced large increases in the numbers of muscarinic receptors and receptors for vasoactive intestinal polypeptide in the salivary glands. Since receptors for vasoactive intestinal polypeptide coexist with muscarinic receptors on the same neurons in this preparation, the results suggest that a drug that alters the sensitivity of one receptor may also affect the sensitivity of the receptor for a costored transmitter and in this way contribute to the therapeutic or side effects of the drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hedlund, B -- Abens, J -- Bartfai, T -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):519-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6132446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Gastrointestinal Hormones/*metabolism ; Male ; Neurotransmitter Agents/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Cholinergic/*drug effects ; Receptors, Muscarinic/analysis/*drug effects ; Salivary Glands/analysis/innervation ; Vasoactive Intestinal Peptide/analysis/*metabolism
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  • 93
    Publication Date: 1983-01-07
    Description: The pathophysiology of autoimmune arthritis was studied by selecting and isolating lines of effector T lymphocytes from rats administered an arthritogenic dose of Mycobacterium tuberculosis in complete Freund's adjuvant to induce adjuvant arthritis. Irradiated rats were intravenously inoculated with a cell line characterized by proliferative reactivity to Mycobacterium tuberculosis and, to a lesser degree, to rat collagen type II. This produced arthritis in all the irradiated rats. Nonirradiated recipients failed to develop arthritis. However, such rats, and those recovering from cell-mediated arthritis, were resistant to subsequent attempts to induce adjuvant arthritis. Lines of T lymphocytes selected for responsiveness to other antigens had no effect. Therefore, a line of T lymphocytes responsive to bacteria or to collagen type II could either induce autoimmune arthritis or serve as an agent of vaccination against it.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holoshitz, J -- Naparstek, Y -- Ben-Nun, A -- Cohen, I R -- NS 18168/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jan 7;219(4580):56-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6336851" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arthritis/*etiology ; Arthritis, Experimental/etiology ; Autoimmune Diseases/*etiology ; Collagen/immunology ; Lymphocyte Activation ; Rats ; T-Lymphocytes/*immunology ; Vaccination ; Whole-Body Irradiation
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  • 94
    Publication Date: 1983-04-15
    Description: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate (a metabolite of the phosphoinositides, lipids involved in membrane receptor function) in the brain. The syndrome was preventable with atropine. The physostigmine doses and concentrations of blood lithium that caused the syndrome are similar to those considered appropriate for psychiatric chemotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Honchar, M P -- Olney, J W -- Sherman, W R -- MH-14677/MH/NIMH NIH HHS/ -- MH-38894/MH/NIMH NIH HHS/ -- NS-05159/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/pharmacology ; Brain Chemistry/drug effects ; Chlorides/adverse effects ; Drug Interactions ; Humans ; Inositol/analogs & derivatives/analysis ; *Inositol Phosphates ; Lithium/*adverse effects ; Lithium Chloride ; Male ; Parasympathomimetics/*adverse effects ; Physostigmine/adverse effects ; Pilocarpine/adverse effects ; Rats ; Rats, Inbred Strains ; Seizures/*chemically induced ; Substance-Related Disorders/*etiology
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  • 95
    Publication Date: 1983-06-03
    Description: A synthetic analog of bovine parathyroid hormone (bPTH), [tyrosine-34] bPTH-(7-34)NH2, was found to inhibit parathyroid hormone action in vivo. When the analog and parathyroid hormone were infused simultaneously to rats at a molar ratio of 200 to 1, the analog inhibited the excretion of urinary phosphate and adenosine 3',5'-monophosphate. When infused alone at the same dose rate, the analog was devoid of agonist activity. The compound was prepared by following design principles developed for inhibitors of parathyroid hormone, and is believed to be the first antagonist of parathyroid hormone that is effective in vivo.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horiuchi, N -- Holick, M F -- Potts, J T Jr -- Rosenblatt, M -- AM11749/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1053-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302844" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cyclic AMP/urine ; Dose-Response Relationship, Drug ; Male ; Parathyroid Hormone/*antagonists & inhibitors/*pharmacology ; Peptide Fragments/*pharmacology ; Phosphates/urine ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 96
    Publication Date: 1983-07-22
    Description: Depletion of polyamines in 9L rat brain tumor cells by treatment with alpha-difluoromethylornithine dramatically altered DNA conformation as measured by viscoelastometry. The reduction of intracellular putrescine and spermidine concentrations to less than 5 percent of their concentrations in control cells decreased the sensitivity of 9L cell DNA to x-irradiation and increased the maximum viscoelastic retardation time of the DNA. Both of these phenomena were reversed by addition of exogenous putrescine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hung, D T -- Marton, L J -- Deen, D F -- Shafer, R H -- CA-13525/CA/NCI NIH HHS/ -- CA-19658/CA/NCI NIH HHS/ -- CA-27343/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 22;221(4608):368-70.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6408733" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Neoplasms/*metabolism ; DNA, Neoplasm/*metabolism ; Eflornithine ; Molecular Conformation ; Ornithine/analogs & derivatives/pharmacology ; Polyamines/*metabolism ; Putrescine/metabolism ; Rats ; Spermidine/metabolism ; Viscosity
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 97
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-07-22
    Description: Protein phosphorylation is a principal regulatory mechanism in the control of almost all cellular processes. The nature of the protein phosphatases that participate in these reactions has been a subject of controversy. Four enzymes, termed protein phosphatases 1, 2A, 2B, and 2C, account for virtually all of the phosphatase activity toward phosphoproteins involved in controlling glycogen metabolism, glycolysis, gluconeogenesis, fatty acid synthesis, cholesterol synthesis, and protein synthesis. The properties, physiological roles, and mechanisms for regulating the four protein phosphatases are reviewed.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ingebritsen, T S -- Cohen, P -- New York, N.Y. -- Science. 1983 Jul 22;221(4608):331-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6306765" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Cyclic AMP/metabolism ; Glycogen/metabolism ; Liver/enzymology ; Muscles/enzymology ; Phosphoprotein Phosphatases/classification/*physiology ; Phosphoproteins/metabolism ; Phosphorylase Phosphatase/metabolism ; Phosphorylation ; Protein Biosynthesis ; Protein Kinases/physiology ; Rabbits ; Rats
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 98
    Publication Date: 1983-09-23
    Description: Evidence is presented that a tumor-derived transforming growth factor is responsible for stimulating bone resorption and causing hypercalcemia in an animal tumor model of the hypercalcemia of malignancy. Both conditioned medium harvested from cultured tumor cells and tumor extracts of the transplantable rat Leydig cell tumor associated with hypercalcemia contained a macromolecular bone resorbing factor with the chemical characteristics of a tumor-derived transforming growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ibbotson, K J -- D'Souza, S M -- Ng, K W -- Osborne, C K -- Niall, M -- Martin, T J -- Mundy, G R -- AM-28149/AM/NIADDK NIH HHS/ -- CA-29537/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 23;221(4617):1292-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6577602" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Bone Resorption ; Calcium ; Cells, Cultured ; Culture Media ; Growth Substances/*physiology ; Hypercalcemia/*etiology ; Leydig Cell Tumor/complications/*physiopathology ; Male ; Neoplasm Proteins/*physiology ; Neoplasms, Experimental/complications/physiopathology ; Peptides/*physiology ; Rats ; Transforming Growth Factors
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 99
    Publication Date: 1983-03-11
    Description: Neurons containing the enzyme aromatic-L-amino-acid decarboxylase (AADC) but lacking either tyrosine hydroxylase or serotonin were found in the spinal cord of neonatal and adult rats by light and electron microscopic immunocytochemistry. The majority of these neurons localized to area X of Rexed contact ependyma. Thus, spinal AADC neurons have the enzymatic capacity to catalyze directly the conversion of the amino acids tyrosine, tryptophan, or phenylalanine to their respective amines tyramine, tryptamine, or phenylethylamine. These amines normally present in the central nervous system may be of potential clinical significance as endogenous psychotomimetics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jaeger, C B -- Teitelman, G -- Joh, T H -- Albert, V R -- Park, D H -- Reis, D J -- HL-07379-04/HL/NHLBI NIH HHS/ -- HL-18974/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Mar 11;219(4589):1233-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6131537" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aromatic-L-Amino-Acid Decarboxylases/*metabolism ; Biogenic Amines/*metabolism ; Brain/*metabolism ; Neurons/enzymology ; Neurotransmitter Agents/biosynthesis ; Rats ; Spinal Cord/*metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 100
    Publication Date: 1983-06-17
    Description: When a solution of collagen molecules, at neutral pH and moderate ionic strength, is warmed from 4 degrees to 30 degrees C, a spontaneous self-assembly process takes place in which native-type collagen fibers are produced. Events occurring during thermally induced fibrillogenesis process can be monitored, in aqueous media and in real time, by Fourier transform infrared spectroscopic techniques. Tentative assignments of observed spectral bands are given.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jakobsen, R J -- Brown, L L -- Hutson, T B -- Fink, D J -- Veis, A -- New York, N.Y. -- Science. 1983 Jun 17;220(4603):1288-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857249" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Collagen/*metabolism ; Connective Tissue/metabolism ; Rats ; Spectrophotometry, Infrared ; Temperature
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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