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  • Rats, Inbred Strains
  • American Association for the Advancement of Science (AAAS)  (55)
  • 1985-1989  (24)
  • 1980-1984  (31)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (55)
Years
Year
  • 1
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    Loss of M2 muscarine receptors in the cerebral cortex in Alzheimer's disease and experimental cholinergic denervation (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-31
    Description: Cerebral cortex samples from patients with Alzheimer's disease and from rats after experimental cholinergic denervation of the cerebral cortex exhibited reductions in the presynaptic marker choline acetyltransferase activity and in the number of M2 muscarine receptors, with no change in the number of M1 receptors. These results are in keeping with evidence that M2 receptors function in cholinergic nerve terminals to regulate the release of acetylcholine, whereas M1 receptors are located on postsynaptic cells and facilitate cellular excitation. New M1-selective agonists and M2-selective antagonists directed at post- or presynaptic sites deserve consideration as potential agents for the treatment of the disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mash, D C -- Flynn, D D -- Potter, L T -- HLO-7188/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 May 31;228(4703):1115-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992249" target="_blank"〉PubMed〈/a〉
    Keywords: Aged ; Alzheimer Disease/*metabolism ; Animals ; Cerebral Cortex/*metabolism ; Choline O-Acetyltransferase/*metabolism ; Cholinergic Fibers/physiology ; Denervation ; Humans ; Male ; Oxotremorine ; Quinuclidinyl Benzilate ; Rats ; Rats, Inbred Strains ; Receptors, Muscarinic/*metabolism ; Synaptic Membranes/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Reduction in oocyte number following prenatal exposure to a diet high in galactose (1981)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1981-12-04
    Description: When pregnant rats were fed a 50 percent galactose diet there was a striking reduction in oocyte number in the offspring. The most prominent effects were noted after exposure to galactose during the premeiotic stages of oogenesis. Prenatal exposure to galactose or its metabolites may contribute to the premature ovarian failure characteristic of human galactosemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Y T -- Mattison, D R -- Feigenbaum, L -- Fukui, H -- Schulman, J D -- New York, N.Y. -- Science. 1981 Dec 4;214(4525):1145-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7302587" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dietary Carbohydrates/*physiology ; Female ; Fetus/drug effects/physiology ; Galactose/*pharmacology ; Maternal-Fetal Exchange ; Oocytes/drug effects/*physiology ; Ovum/*physiology ; Pregnancy ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Corticotropin-releasing factor stimulates secretion of melanocyte-stimulating hormone from the rat pituitary (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-07-02
    Description: Administration of synthetic ovine corticotropin-releasing factor led to rapid, parallel increases in adrenocorticotropin and alpha-melanocyte-stimulating hormone concentrations in rat plasma. Prior treatment with dexamethasone almost completely blocked the adrenocorticotropin response but not the increase in melanocyte-stimulating hormone. These data demonstrate that corticotropin-releasing factor is a potent stimulator not only of adrenocorticotropin secretion from the corticotrophs of the anterior pituitary gland but also of peptide secretion from the intermediate lobe. Such data suggest that melanocyte-stimulating hormone and beta-endorphin play a role in the physiological response to stress.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Proulx-Ferland, L -- Labrie, F -- Dumont, D -- Cote, J -- Coy, D H -- Sveiraf, J -- New York, N.Y. -- Science. 1982 Jul 2;217(4554):62-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6283632" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/blood ; Animals ; Castration ; Corticotropin-Releasing Hormone/*pharmacology ; Dexamethasone/pharmacology ; Female ; Melanocyte-Stimulating Hormones/blood/*secretion ; Pituitary Gland/drug effects/*secretion ; Pituitary Gland, Anterior/secretion ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Insulin receptor antiserum and plant lectins mimic the direct effects of insulin on nuclear envelope phosphorylation (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-07-29
    Description: Insulin directly inhibits protein phosphorylation in isolated rat liver nuclear envelopes. In the present studies, an antiserum to insulin receptor as well as the plant lectins concanavalin A and phytohemagglutinin mimicked insulin action in isolated nuclear envelopes. These studies suggest that insulin and agents that mimic it may directly regulate nuclear functions.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Purrello, F -- Burnham, D B -- Goldfine, I D -- AM 06659/AM/NIADDK NIH HHS/ -- AM 26667/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 29;221(4609):462-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6346487" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Concanavalin A/pharmacology ; Female ; Immune Sera ; Insulin/*pharmacology ; Lectins/*pharmacology ; Nuclear Envelope/*drug effects/metabolism ; Phosphorylation ; Phytohemagglutinins/pharmacology ; Rats ; Rats, Inbred Strains ; Receptor, Insulin/*immunology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    A selective imidazobenzodiazepine antagonist of ethanol in the rat (1986)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1986-12-05
    Description: Ethanol, at pharmacologically relevant concentrations of 20 to 100 mM, stimulates gamma-aminobutyric (GABA) receptor-mediated uptake of 36Cl-labeled chlorine into isolated brain vesicles. One drug that acts at GABA-benzodiazepine receptors, the imidazobenzodiazepine Ro15-4513, has been found to be a potent antagonist of ethanol-stimulated 36Cl- uptake into brain vesicles, but it fails to antagonize either pentobarbital- or muscimol-stimulated 36Cl- uptake. Pretreatment of rats with Ro15-4513 blocks the anticonflict activity of low doses of ethanol (but not pentobarbital) as well as the behavioral intoxication observed with higher doses of ethanol. The effects of Ro15-4513 in antagonizing ethanol-stimulated 36Cl- uptake and behavior are completely blocked by benzodiazepine receptor antagonists. However, other benzodiazepine receptor inverse agonists fail to antagonize the actions of ethanol in vitro or in vivo, suggesting a novel interaction of Ro15-4513 with the GABA receptor-coupled chloride ion channel complex. The identification of a selective benzodiazepine antagonist of ethanol-stimulated 36Cl- uptake in vitro that blocks the anxiolytic and intoxicating actions of ethanol suggests that many of the neuropharmacologic actions of ethanol may be mediated via central GABA receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Suzdak, P D -- Glowa, J R -- Crawley, J N -- Schwartz, R D -- Skolnick, P -- Paul, S M -- New York, N.Y. -- Science. 1986 Dec 5;234(4781):1243-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3022383" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anxiety/drug effects ; Azides/*pharmacology ; Benzodiazepines/*pharmacology ; Chlorides/metabolism ; Ethanol/*antagonists & inhibitors ; Flumazenil/pharmacology ; Male ; Pyrazoles/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, GABA-A/drug effects ; Synaptosomes/drug effects
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    GM1 ganglioside treatment facilitates behavioral recovery from bilateral brain damage (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-07-20
    Description: Adult rats with bilateral lesions of the caudate nucleus were treated with GM1 ganglioside. Although animals injected with a control solution were severely impaired in their ability to learn a complex spatial task, those treated with ganglioside were able to learn spatial reversals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sabel, B A -- Slavin, M D -- Stein, D G -- New York, N.Y. -- Science. 1984 Jul 20;225(4659):340-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6740316" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*drug effects ; Brain Injuries/*drug therapy/psychology ; Caudate Nucleus/drug effects/injuries ; G(M1) Ganglioside/pharmacology/*therapeutic use ; Gangliosides/*therapeutic use ; Humans ; Learning/drug effects ; Male ; Rats ; Rats, Inbred Strains
    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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  • 7
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    Imaging of phosphorescence: a novel method for measuring oxygen distribution in perfused tissue (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-09-23
    Description: The imaging of phosphorescence provides a method for monitoring oxygen distribution within the vascular system of intact tissues. Isolated rat lives were perfused through the portal vein with media containing palladium coproporphyrin, which phosphoresced and was used to image the liver at various perfusion rates. Because oxygen is a powerful quenching agent for phosphors, the transition from well-perfused liver to anoxia (no flow of oxygen) resulted in large increases of phosphorescence. During stepwise restoration of oxygen flow, the phosphorescence images showed marked heterogeneous patterns of tissue reoxygenation, which indicated that there were regional inequalities in oxygen delivery.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rumsey, W L -- Vanderkooi, J M -- Wilson, D F -- GM 21524/GM/NIGMS NIH HHS/ -- GM 36393/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1988 Sep 23;241(4873):1649-51.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, Philadelphia 19104.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3420417" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Coproporphyrins ; Liver Circulation ; *Luminescence ; Male ; Oxygen/*analysis ; Palladium ; Perfusion ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Expression of transducin in retinal rod photoreceptor outer segments (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Roof, D J -- Heth, C A -- EY05790/EY/NEI NIH HHS/ -- EY06514/EY/NEI NIH HHS/ -- New York, N.Y. -- Science. 1988 Aug 12;241(4867):845-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Berman-Gund Laboratory, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3136548" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Darkness ; GTP-Binding Proteins/*biosynthesis ; Light ; Membrane Proteins/*biosynthesis/isolation & purification ; Photoreceptor Cells/*metabolism ; Rats ; Rats, Inbred Strains ; Rod Cell Outer Segment/*metabolism/radiation effects ; Species Specificity ; Transducin
    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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  • 9
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    Postponement of satiety by blockade of brain cholecystokinin (CCK-B) receptors (1989)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1989-09-29
    Description: Exogenous cholecystokinin (CCK) decreases food intake and causes satiety in animals and man. However, it has not been established that endogenous CCK causes satiety or whether the response is mediated by peripheral-type (CCK-A) or brain-type (CCK-B) receptors. The development of potent and selective antagonists for CCK-A (MK-329) and CCK-B (L-365,260) receptors now allows these issues to be addressed. The CCK-A antagonist MK-329 and the CCK-B antagonist L-365,260 increased food intake in partially satiated rats and postponed the onset of satiety; however, L-365,260 was 100 times more potent than MK-329 in increasing feeding and preventing satiety. These results suggest that endogenous CCK causes satiety by an agonist action on CCK-B receptors in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dourish, C T -- Rycroft, W -- Iversen, S D -- New York, N.Y. -- Science. 1989 Sep 29;245(4925):1509-11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Merck Sharp & Dohme Research Laboratories, Neuroscience Research Center, Terlings Park, Harlow, Essex, England.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2781294" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzodiazepines/pharmacology ; Benzodiazepinones/pharmacology ; Brain/drug effects/*physiology ; Cholecystokinin/antagonists & inhibitors/*physiology ; Devazepide ; Male ; *Phenylurea Compounds ; Rats ; Rats, Inbred Strains ; Receptors, Cholecystokinin/drug effects/*physiology ; Satiation/*physiology
    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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  • 10
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    Contributions of quisqualate and NMDA receptors to the induction and expression of LTP (1988)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1988-12-23
    Description: The contributions of two subclasses of excitatory amino acid transmitter receptors to the induction and expression of long-term potentiation (LTP) were analyzed in hippocampal slices. The quisqualate/kainate receptor antagonist DNQX (6,7-dinitro-quinoxaline-2,3-dione) blocked 85% of the evoked field potential, leaving a small response that was sensitive to D-AP5 (D-2-amino-5-phosphonopentanoate), an N-methyl-D-aspartate (NMDA) receptor blocker. This residual D-AP5-sensitive response was of comparable size in control and previously potentiated inputs. High-frequency stimulation in the presence of DNQX did not result in the development of robust LTP. Washout of the drug, however, revealed the potentiation effect. Thus NMDA-mediated responses can induce, but are not greatly affected by, LTP; non-NMDA receptors, conversely, mediate responses that are not needed to elicit LTP but that are required for its expression.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, D -- Joly, M -- Lynch, G -- New York, N.Y. -- Science. 1988 Dec 23;242(4886):1694-7.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for the Neurobiology of Learning and Memory, University of California, Irvine 92717.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2904701" target="_blank"〉PubMed〈/a〉
    Keywords: 2-Amino-5-phosphonovalerate ; Animals ; Electric Conductivity ; Electric Stimulation ; Evoked Potentials/drug effects ; Hippocampus/*physiology ; Magnesium/pharmacology ; Male ; Membrane Potentials/drug effects ; Quinoxalines/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, AMPA ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/drug effects/*physiology ; Synapses/*physiology ; Valine/analogs & derivatives/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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