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  • Rats, Inbred Strains  (9)
  • American Association for the Advancement of Science (AAAS)  (9)
  • 1980-1984  (9)
  • 1982  (9)
Collection
Keywords
Publisher
  • American Association for the Advancement of Science (AAAS)  (9)
Years
  • 1980-1984  (9)
Year
  • 1
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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
    Published by American Association for the Advancement of Science (AAAS)
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  • 2
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    Ethanol in low doses augments calcium-mediated mechanisms measured intracellularly in hippocampal neurons (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-01-15
    Description: The electrophysiological effects of ethanol in low doses (5 to 20 millimoles per liter or 23 to 92 milligrams per 100 milliliters) were examined intracellularly in CA1 cells of rat hippocampus in vitro. Inhibitory and excitatory postsynaptic potentials were increased when ethanol was applied to the respective synaptic terminal regions. Postsynaptically, ethanol caused a moderate hyperpolarization with increased membrane conductance, even when synaptic transmission was blocked. Ethanol augmented the hyperpolarization that followed repetitive firing or that followed the eliciting of calcium spikes in the presence of tetrodotoxin, but not the rapid afterhyperpolarization in calcium-free medium. Ethanol appears to augment calcium-mediated mechanisms both pre- and postsynaptically.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Carlen, P L -- Gurevich, N -- Durand, D -- R01 NS16660-01/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Jan 15;215(4530):306-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7053581" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/physiology ; Electric Conductivity ; Ethanol/*pharmacology ; Hippocampus/*drug effects/physiology ; Male ; Membrane Potentials/drug effects ; Potassium/physiology ; Rats ; Rats, Inbred Strains ; Synaptic Membranes/drug effects ; Tetrodotoxin/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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  • 3
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    Modulation of striatal dopaminergic function by local injection of 5'-N-ethylcarboxamide adenosine (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-10-01
    Description: Rats rotated to the left when 5'-N-ethylcarboxamide adenosine (NECA) was injected into the left caudate nucleus and apomorphine was administered subcutaneously. The combination of NECA and apomorphine was more potent than L-(phenylisopropyl)adenosine and apomorphine in eliciting rotation, suggesting the involvement of adenosine receptors of the Ra type. The response was reduced when 2',5'-dideoxyadenosine was injected along with NECA into the caudate nucleus or when theorphylline was given intraperitoneally. Higher doses of apomorphine elicited a self-mutilatory response after the injection of NECA into the caudate nucleus. These results suggest that adenosine may be involved in the modulation of dopaminergic function in the striatum.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Green, R D -- Proudfit, H K -- Yeung, S M -- New York, N.Y. -- Science. 1982 Oct 1;218(4567):58-61.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7123218" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/administration & dosage/*analogs & derivatives/pharmacology ; Adenosine-5'-(N-ethylcarboxamide) ; Animals ; Apomorphine/pharmacology ; Caudate Nucleus/*physiology ; Corpus Striatum/*physiology ; Dopamine/*physiology ; Injections ; Kinetics ; Male ; Motor Activity/drug effects ; Rats ; Rats, Inbred Strains ; Rotation ; Vasodilator Agents/*pharmacology
    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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  • 4
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    Suppression of ovulation in the rat by an orally active antagonist of luteinizing hormone-releasing hormone (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-10-08
    Description: A synthetic antagonist of luteinizing hormone-releasing hormone blocked ovulation in rats in a dose-dependent manner when given by gavage on the afternoon of proestrus. Ovulation was delayed for at least 1 day in all animals given 2 milligrams of antogonist and in some of the animals treated with 1 or 0.5 milligram. Oral administration of 2 milligrams also blocked the preovulatory surge of luteinizing hormone. This demonstration that antagonists of luteinizing hormone-releasing hormone can have oral antiovulatory activity clearly enhances their therapeutic potential.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nekola, M B -- Horvath, A -- Ge, L J -- Coy, D H -- Schally, A V -- HD-0-2831/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1982 Oct 8;218(4568):160-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6750790" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Female ; Gonadotropin-Releasing Hormone/*analogs & derivatives/pharmacology ; Luteinizing Hormone/secretion ; Ovulation/*drug effects ; Pregnancy ; Proestrus/drug effects ; 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
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Brain injury causes a time-dependent increase in neuronotrophic activity at the lesion site (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-08-27
    Description: A cavity was made in the brain (entorhinal cortex) of developing or adult rats, and a small piece of Gelfoam was emplaced to collect fluid secreted into the wound. The neuronotrophic activity of the fluid was assayed with sympathetic and parasympathetic neurons in culture. The results show that wounds in the brain of developing or adult rats stimulate the accumulation of neuronotrophic factors and that the activity of these factors increases over the first few days after infliction of the damage.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nieto-Sampedro, M -- Lewis, E R -- Cotman, C W -- Manthorpe, M -- Skaper, S D -- Barbin, G -- Longo, F M -- Varon, S -- AG-00538/AG/NIA NIH HHS/ -- MH-19691/MH/NIMH NIH HHS/ -- NS-16349/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Aug 27;217(4562):860-1.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7100931" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic Fibers/physiology ; Animals ; Brain/*physiology ; Brain Injuries/*physiopathology ; Cell Survival/drug effects ; Cells, Cultured ; Cholinergic Fibers/physiology ; Kinetics ; Nerve Growth Factors/*metabolism/pharmacology ; *Nerve Regeneration ; Rats ; Rats, Inbred Strains ; Wound Healing
    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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    Hypotensive effect of fasting: possible involvement of the sympathetic nervous system and endogenous opiates (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-08-20
    Description: Fasting lowers blood pressure to a greater extent in spontaneously hypertensive rats than in normotensive rats. While fasting reduced cardiac sympathetic activity to an equivalent extent in both groups of animals, only in the hypertensive rats did fasting elicit an opiate-mediated vasodepressor response that was independent of sympathetic withdrawal. Both sympathetic nervous system suppression and endogenous opiate activation, therefore, may contribute to the hypotensive effect of fasting in the spontaneously hypertensive rat.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Einhorn, D -- Young, J B -- Landberg, L -- AM 20378/AM/NIADDK NIH HHS/ -- HL 24084/HL/NHLBI NIH HHS/ -- RR 76/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1982 Aug 20;217(4561):727-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7100917" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Blood Pressure/drug effects ; Endorphins/*physiology ; *Fasting ; Hypertension/physiopathology ; Male ; Myocardium/metabolism ; Naltrexone/pharmacology ; Norepinephrine/metabolism ; Rats ; Rats, Inbred Strains ; Sympathetic Nervous System/*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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  • 7
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    Neonatal treatment with antiserum to prolactin lowers blood pressure in rats (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-07-09
    Description: Prolactin administration reportedly increases blood pressure in rats and rabbits. To study the effects of prolactin deficiency on blood pressure, rats were given saline, normal rabbit serum, or rabbit antiserum to rat prolactin on postnatal days 2 to 5. Both males and females given antiserum had significantly lower blood pressure at 14 weeks than rats given saline or normal rabbit serum. Blood pressure differences between females given antiserum and females given saline disappeared during and following pregnancy. The antiserum also lowered the concentration of prolactin in plasma 49 percent in males and decreased the prolactin response to ether stress in both sexes. These results suggest that endogenous prolactin is involved in blood pressure regulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mills, D E -- Buckman, M T -- Peake, G T -- New York, N.Y. -- Science. 1982 Jul 9;217(4555):162-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7089550" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; *Blood Pressure ; Female ; Immune Sera/pharmacology ; Male ; Pregnancy ; Pregnancy, Animal ; Prolactin/blood/immunology/*physiology ; Rabbits ; Rats ; Rats, Inbred Strains ; Sex Characteristics ; Sodium Chloride/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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  • 8
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    Lesion-induced sprouting in the rat dentate gyrus is inhibited by repeated ethanol administration (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-11-19
    Description: The effect of ethanol on hippocampal axonal sprouting was studied with a histochemical technique for identifying acetylcholinesterase. Unilateral lesion of the entorhinal cortex in adult rats produced an increase in the density of acetylcholinesterase staining in the outer molecular layer and a concomitant increase in the width of the pale-staining commissural-associational zone of the dentate gyrus. Other rats were given ethanol (11.3 +/- 0.45 grams per kilogram) for 2 weeks before and 9 days after receiving the lesion. Ethanol abolished the expansion of the commissural-associated zone. The effect of ethanol on sprouting axons suggests that it may inhibit recovery of function after brain injury.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉West, J R -- Lind, M D -- Demuth, R M -- Parker, E S -- Alkana, R L -- Cassell, M -- Black, A C Jr -- AA-03884/AA/NIAAA NIH HHS/ -- New York, N.Y. -- Science. 1982 Nov 19;218(4574):809-10.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7134977" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/drug effects/*physiology ; Ethanol/*pharmacology ; Female ; Hippocampus/drug effects/*physiology ; 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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  • 9
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    Biotin enhances guanylate cyclase activity (1982)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1982-06-18
    Description: Biotin and its analog, (+)-biotin-p-nitrophenyl ester enhanced guanylate cyclase activity two- to threefold in rat liver, kidney, colon, cerebellum, and heart. Dose-response relationships revealed that at concentrations as low as 1 micromolar, both biotin and its analog caused maximal augmentation of guanylate cyclase activity. These data suggest a role for the activation of guanylate cyclase in the mechanism of action of this vitamin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vesely, D L -- New York, N.Y. -- Science. 1982 Jun 18;216(4552):1329-30.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6123152" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biotin/analogs & derivatives/*pharmacology ; Cerebellum/enzymology ; Colon/enzymology ; Guanylate Cyclase/*metabolism ; Kidney/enzymology ; Kinetics ; Liver/enzymology ; Myocardium/enzymology ; 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
    Published by American Association for the Advancement of Science (AAAS)
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