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  • Artikel  (20)
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  • 1
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-07-02
    Beschreibung: Gastric acid secretion has been thought to depend on histamine stimulation of the parietal cell. However, in the 2-week-old rat neither exogenous histamine nor the H-2 receptor agonist impromidine stimulates acid secretion, whereas pentagastrin and the cholinergic agent bethanechol are potent stimuli. At this age, the effect of pentagastrin in acid secretion is not blocked by the H-2 receptor antagonist cimetidine, nor is it potentiated by impromidine. These data suggest that, in the rat pup, the acid secretory response to pentagastrin and cholinergic agents occurs before the histamine-mediated system is functional and operates independently of the actions of histamine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ackerman, S H -- K1-MH00077/MH/NIMH NIH HHS/ -- R01-AM-18804/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1982 Jul 2;217(4554):75-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6211765" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Aging ; Animals ; Bethanechol Compounds/pharmacology ; Gastric Juice/drug effects/*secretion ; Gastric Mucosa/growth & development ; Guanidines/pharmacology ; Histamine/pharmacology ; Imidazoles/pharmacology ; Impromidine ; Pentagastrin/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Histamine H2/drug effects
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 2
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-01-08
    Beschreibung: (+/-)-N-Allylnormetazocine is a benzomorphan opioid with psychotomimetic effects. The pure stereoisomers of this compound, as well as the racemic mixture, were compared to phencyclidine for their behavioral effects on squirrel monkeys and rats trained to discriminate phencyclidine from saline. Dose-response determinations were made for responses to phencyclidine, to a racemic mixture of N-allylnormetazocine, and to the pure levo and dextro isomers of N-allylnormetazocine. In both rats and monkeys, the dextro isomer and the racemic mixture produced dose-dependent responses appropriate for phencyclidine; the levo isomer did not produce the responses appropriate for phencyclidine at any of the doses tested. In both species, the levo isomer was more potent than the dextro isomer in decreasing the rate of responding. Thus racemic N-allylnormetazocine is a mixture of compounds that produce different behavioral effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Brady, K T -- Balster, R L -- May, E L -- DA-00490/DA/NIDA NIH HHS/ -- DA-01442/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1982 Jan 8;215(4529):178-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6274022" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Behavior, Animal/*drug effects ; Male ; Naloxone/pharmacology ; Phenazocine/*analogs & derivatives/pharmacology ; Phencyclidine/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Opioid/drug effects ; Saimiri ; Stereoisomerism ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 3
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-10-08
    Beschreibung: Rats whose pregnancies were surgically terminated on day 17 of gestation were injected with morphine, morphine plus naloxone hydrochloride, or saline, and then tested for maternal responsiveness toward foster young. Morphine treatment alone significantly disrupted the rate of onset and quality of maternal responsiveness. Concurrent administration of naloxone to morphine-injected rats reinstated the rapid onset of behavioral responsiveness toward foster young, such that the responsiveness of the rats treated with both morphine and naloxone was indistinguishable from that shown by saline-injected controls. The disruptive effects of morphine did not appear to result from a general reduction in activity levels as measured in an open-field apparatus. These findings suggest that the normal onset and maintenance of maternal behavior in the rat may be regulated by endogenous opiates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bridges, R S -- Grimm, C T -- New York, N.Y. -- Science. 1982 Oct 8;218(4568):166-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7123227" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Behavior, Animal/*drug effects ; Drug Antagonism ; Female ; Morphine/*pharmacology ; Naloxone/*pharmacology ; Pregnancy ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 4
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-01-15
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 5
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-10-01
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 6
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-07-02
    Beschreibung: Inosine peripherally administered to rats markedly suppressed spontaneous food intake and food intake induced by diazepam, muscimol, insulin, and food deprivation. The purines 2-deoxyguanosine and 2-deoxyinosine also suppressed food deprivation-induced feeding, whereas 7-methylinosine, which does not bind to the benzodiazepine binding site in vitro, had no effect on food intake when compared with controls. These results suggest that purines may represent endogenous substances that regulate food intake through interactions with the benzodiazepine receptor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Levine, A S -- Morley, J E -- New York, N.Y. -- Science. 1982 Jul 2;217(4554):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7046046" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Appetite/*drug effects ; Deoxyguanosine/pharmacology ; Diazepam/pharmacology ; Eating/*drug effects ; Food Deprivation ; Inosine/analogs & derivatives/pharmacology ; Insulin/pharmacology ; Male ; Muscimol/pharmacology ; Purines/*pharmacology ; Rats ; Rats, Inbred Strains ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 7
    Publikationsdatum: 1982-10-08
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 8
    Publikationsdatum: 1982-08-27
    Beschreibung: 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〉
    Schlagwort(e): 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
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 9
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    Unbekannt
    American Association for the Advancement of Science (AAAS)
    Publikationsdatum: 1982-10-08
    Beschreibung: Topical application of convulsants to the rat sensorimotor cortex in concentrations sufficient to cause repetitive focal motor seizures resulted in acute neuropathology (dark cell neuronal degeneration and spongiform neurophil changes) involving both the cortical seizure focus and certain thalamic nuclei within seizure pathways. Changes in the cortex were localized primarily in layer IV and those in the thalamus in nuclei having reciprocal connections with the cortical focus. The spongiform neuropil changes consisted of massively dilated presynaptic axon terminals in the cortex and postsynaptic dendrites in the thalamus. The dendritic and dark cell changes resemble the excitotoxic damage caused by glutamate and aspartate. Since these putative transmitters may be released locally from recurrent collaterals and remotely from corticothalamic axons, excessive release of glutamate or aspartate may account for the changes in both sites. The abnormal axons in sensory cortex appear to be terminals of thalamocortical neurons. Swelling of these axons may be caused by excessive anti- and orthodromic firing in the course of focal motor seizures.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Collins, R C -- Olney, J W -- MH-38894/MH/NIMH NIH HHS/ -- NS-09156/NS/NINDS NIH HHS/ -- NS-14834/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Oct 8;218(4568):177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7123229" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Axons/ultrastructure ; Cerebral Cortex/*physiopathology/ultrastructure ; Microscopy, Electron ; Neurons/physiology/ultrastructure ; Rats ; Rats, Inbred Strains ; Seizures/*physiopathology ; Thalamus/*physiopathology
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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  • 10
    Publikationsdatum: 1982-01-15
    Beschreibung: Autoradiograms prepared from adult rat brains demonstrate that nerve cells and neuropil in different brain regions selectively concentrate and retain intravenously administered triiodothyronine, by mechanisms susceptible to saturation with excess triiodothyronine. A neuroregulatory role for thyroid hormones, strongly supported by the observations, may account for their marked effects on behavior and the activity of the autonomic nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Dratman, M B -- Futaesaku, Y -- Crutchfield, F L -- Berman, N -- Payne, B -- Sar, M -- Stumpf, W E -- HD03110/HD/NICHD NIH HHS/ -- MH29549/MH/NIMH NIH HHS/ -- NS09914/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1982 Jan 15;215(4530):309-12.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7053582" target="_blank"〉PubMed〈/a〉
    Schlagwort(e): Animals ; Autoradiography ; Brain/cytology/*metabolism ; Brain Mapping ; Male ; Rats ; Rats, Inbred Strains ; Triiodothyronine/*metabolism
    Print ISSN: 0036-8075
    Digitale ISSN: 1095-9203
    Thema: Biologie , Chemie und Pharmazie , Informatik , Medizin , Allgemeine Naturwissenschaft , Physik
    Standort Signatur Erwartet Verfügbarkeit
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