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  • Articles  (63)
  • Rats, Inbred Strains  (63)
  • 1985-1989  (30)
  • 1980-1984  (33)
  • 1925-1929
  • 1985  (30)
  • 1983  (33)
  • Physics  (63)
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  • Articles  (63)
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  • 1985-1989  (30)
  • 1980-1984  (33)
  • 1925-1929
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  • 1
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    Regulation of carcinogen metabolism in the rat ovary by the estrous cycle and gonadotropin (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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  • 2
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    Pimozide blocks establishment but not expression of amphetamine-produced environment-specific conditioning (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 3
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    Direct in vivo monitoring of dopamine released from two striatal compartments in the rat (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 4
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    Scientist sues over genetically impure mice (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 5
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    Adenosine receptors: autoradiographic evidence for their location on axon terminals of excitatory neurons (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    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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    Vasoactive intestinal polypeptide and muscarinic receptors: supersensitivity induced by long-term atropine treatment (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 7
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    Systemic cholinergic agents induce seizures and brain damage in lithium-treated rats (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    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
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 8
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    Inhibition of gastric acid secretion in rats by intracerebral injection of corticotropin-releasing factor (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-25
    Description: Intracisternal injection of ovine corticotropin-releasing factor (CRF) into the pylorus-ligated rat or the rat with gastric fistula resulted in a dose-dependent inhibition of gastric secretion stimulated with pentagastrin or thyrotropin-releasing hormone. When injected into the lateral hypothalamus--but not when injected into the cerebral cortex--CRF suppressed pentagastrin-stimulated acid secretion. The inhibitory effect of CRF was blocked by vagotomy and adrenalectomy but not by hypophysectomy or naloxone treatment. These results indicate that CRF acts within the brain to inhibit gastric acid secretion through vagal and adrenal mechanisms and not through hypophysiotropic effects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tache, Y -- Goto, Y -- Gunion, M W -- Vale, W -- River, J -- Brown, M -- AM30110/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Nov 25;222(4626):935-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6415815" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Brain/*drug effects ; Cerebral Cortex/drug effects ; Corticotropin-Releasing Hormone/administration & dosage/*pharmacology ; Dose-Response Relationship, Drug ; Gastric Acid/*secretion ; Hypophysectomy ; Hypothalamus/drug effects ; Male ; Pentagastrin/antagonists & inhibitors ; Rats ; Rats, Inbred Strains ; Thyrotropin-Releasing Hormone/antagonists & inhibitors ; Vagotomy
    Print ISSN: 0036-8075
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  • 9
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    Insulin-like growth factors: a role in growth hormone negative feedback and body weight regulation via brain (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-01
    Description: Intracerebroventricular administration of ILA's, a preparation enriched in insulin-like growth factors, caused a marked decrease in growth hormone secretory episodes and in body weight associated with reduced food intake over 24 hours. Central injection of insulin and bovine serum albumin had no such effects. These findings suggest that insulin-like growth factors play a role in growth hormone negative feedback and body weight regulation at the level of the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tannenbaum, G S -- Guyda, H J -- Posner, B I -- New York, N.Y. -- Science. 1983 Apr 1;220(4592):77-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6338593" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Body Weight/*drug effects ; Brain/drug effects/*physiology ; Eating/drug effects ; Growth Hormone/antagonists & inhibitors/blood/*physiology ; Insulin/blood/*pharmacology ; Male ; Peptides/*pharmacology ; Rats ; Rats, Inbred Strains ; Somatomedins/*pharmacology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
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    Potent interaction between glucocorticoids and growth hormone-releasing factor in vivo (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-05
    Description: Administration of dexamethasone significantly enhanced the pituitary growth hormone response to growth hormone-releasing factor in intact as well as adrenalectomized rats. Thus the inhibitory effects of glucocorticosteroids on somatic growth which involve an interaction of these steroids and growth hormone at a peripheral level may also involve a modification of pathways within the central nervous system that regulate normal growth hormone secretion.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wehrenberg, W B -- Baird, A -- Ling, N -- AM-18811/AM/NIADDK NIH HHS/ -- HD 09690/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 5;221(4610):556-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6408735" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Dexamethasone/pharmacology ; Drug Interactions ; Glucocorticoids/*pharmacology ; Growth Hormone/blood/secretion ; Growth Hormone-Releasing Hormone/*pharmacology ; Male ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 11
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    Increased brain size and cellular content in infant rats treated with an opiate antagonist (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-16
    Description: From birth to day 21, rat offspring received daily injections of naltrexone at a dosage that blocked morphine-induced analgesia 24 hours a day. At 21 days, body, brain, and cerebellar weights of naltrexone-injected animals were 18, 11, and 5 percent greater than corresponding control weights. In addition, morphometric analysis of the cerebrum revealed a somatosensory cortex that was 18 percent thicker than that of the controls. The cerebellum of naltrexone-treated rats was 41 percent larger in total area and contained at least 70 percent more glial cells and 30 percent more granule neurons. Neurons derived prenatally were unaffected by drug treatment. These results show that naltrexone can stimulate body and brain growth in rats and suggest a role for the endorphin and opiate receptor system in development.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagon, I S -- McLaughlin, P J -- New York, N.Y. -- Science. 1983 Sep 16;221(4616):1179-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612331" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Animals, Newborn ; Body Weight/drug effects ; Brain/*drug effects/growth & development/ultrastructure ; Cerebellum/drug effects ; Morphine/*antagonists & inhibitors ; Naloxone/*analogs & derivatives ; Naltrexone/*pharmacology ; Neuroglia/drug effects ; Organ Size/drug effects ; Rats ; Rats, Inbred Strains ; Somatosensory Cortex/drug effects
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 12
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    Interrelated striated elements in vestibular hair cells of the rat (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-06
    Description: Unusual fixation procedures revealed a series of interrelated striated organelles in type I and type II vestibular hair cells of the rat; these organelles seemed to be less well developed in cochlear hair cells. The findings suggest that contractile elements may play a role in sensory transduction in the inner ear, particularly in the vestibular system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ross, M D -- Bourne, C -- New York, N.Y. -- Science. 1983 May 6;220(4597):622-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6682246" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/physiology ; Animals ; Cell Membrane/ultrastructure ; Cytoskeleton/ultrastructure ; Hair Cells, Auditory/*ultrastructure ; Microscopy, Electron ; Organoids/ultrastructure ; Rats ; Rats, Inbred Strains
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 13
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    Nicotinic cholinergic receptor binding sites in the brain: regulation in vivo (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-08
    Description: Tritiated acetylcholine was used to measure binding sites with characteristics of nicotinic cholinergic receptors in rat brain. Regulation of the binding sites in vivo was examined by administering two drugs that stimulate nicotinic receptors directly or indirectly. After 10 days of exposure to the cholinesterase inhibitor diisopropyl fluorophosphate, binding of tritiated acetylcholine in the cerebral cortex was decreased. However, after repeated administration of nicotine for 10 days, binding of tritiated acetylcholine in the cortex was increased. Saturation analysis of tritiated acetylcholine binding in the cortices of rats treated with diisopropyl fluorophosphate or nicotine indicated that the number of binding sites decreased and increased, respectively, while the affinity of the sites was unaltered.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schwartz, R D -- Kellar, K J -- 507 RR05360-20/RR/NCRR NIH HHS/ -- GM07443/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):214-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828889" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/metabolism ; Animals ; Brain/*physiology ; Brain Chemistry/drug effects ; Cerebral Cortex/analysis/physiology ; Isoflurophate/pharmacology ; Male ; Nicotine/metabolism/pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Cholinergic/*physiology ; Receptors, Nicotinic/analysis/*physiology
    Print ISSN: 0036-8075
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  • 14
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    Retinal capillaries: basement membrane thickening by galactosemia prevented with aldose reductase inhibitor (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-16
    Description: A twofold thickening of capillary basement membranes of rat retinas resulting from dietary galactose was prevented by sorbinil, an inhibitor of aldose reductase. Since the basement membrane thickening was ultrastructurally similar to that typical of diabetic retinopathy, it may indicate changes in vessel permeability and susceptibility to hemorrhage. Galactosemic rats should be useful models for studying basement membrane-related complications of diabetes and for examining the potential biochemical regulation of basement membrane synthesis by aldose reductase inhibitors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robison, W G Jr -- Kador, P F -- Kinoshita, J H -- New York, N.Y. -- Science. 1983 Sep 16;221(4616):1177-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6612330" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Basement Membrane/*pathology ; Capillaries/pathology ; Diabetic Retinopathy/etiology ; Disease Models, Animal ; Galactosemias/drug therapy/*pathology ; Imidazoles/*therapeutic use ; *Imidazolidines ; Male ; Rats ; Rats, Inbred Strains ; Retinal Vessels/*pathology
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  • 15
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    Single-channel fluctuations in bimolecular lipid membranes induced by rat olfactory epithelial homogenates (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-13
    Description: Chemosensitive single-channel fluctuations were observed to be induced in essentially solvent-free lipid bimolecular membranes by the addition of sonicated homogenates of rat olfactory epithelium. The chemosensitive channels were not observed when respiratory epithelium homogenates were used instead. Ionic selectivity is consistent with potassium ions as the charge carrier. These channels may be associated with the initial events of chemoreception in the rat olfactory epithelium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Vodyanoy, V -- Murphy, R B -- New York, N.Y. -- Science. 1983 May 13;220(4598):717-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301014" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anura ; Chemoreceptor Cells/physiology ; Epithelium/physiology ; Ion Channels/*drug effects ; Male ; Membranes/drug effects ; Olfactory Mucosa/*physiology ; Rats ; Rats, Inbred Strains ; Smell/physiology
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  • 16
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    Dopamine modulation of the effects of gamma-aminobutyric acid on substantia nigra pars reticulata neurons (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-08
    Description: Studies were conducted to assess whether basal ganglia output neurons originating in the substantia nigra pars reticulata might be affected by dopamine released from dendrites of neighboring substantia nigra pars compacta neurons. Dopamine applied by iontophoresis increased the baseline firing rates of approximately half of the substantia nigra pars reticulata cells tested. The more significant finding, unrelated to the increase in firing, was the ability of dopamine to attenuate the inhibitory responses of these cells to iontophoretically applied gamma-aminobutyric acid. These findings suggest a role for dopamine as a neuromodulator and further suggest that it can act at sites beyond the striatum to modify transmission from the basal ganglia to motor nuclei.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waszcak, B L -- Walters, J R -- New York, N.Y. -- Science. 1983 Apr 8;220(4593):218-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6828891" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials/drug effects ; Animals ; Dopamine/*pharmacology ; Iontophoresis ; Male ; Neurons/*drug effects ; Norepinephrine/pharmacology ; Rats ; Rats, Inbred Strains ; Substantia Nigra/*drug effects ; gamma-Aminobutyric Acid/*pharmacology
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  • 17
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    Effects of tyrosine administration on serum biopterin in normal controls and patients with Parkinson's disease (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-01-07
    Description: After administration of tyrosine, total concentration of biopterin, the cofactor for tyrosine hydroxylase, was increased in the striatum, adrenal glands, and serum of rats, and in the serum of humans. Serum biopterin is lower in patients with Parkinson's disease than in normal controls. After oral administration of tyrosine, the increase in serum biopterin concentration was smaller in patients with Parkinson's disease (less than twofold) than in healthy controls (three-to sevenfold). These results suggest that tyrosine may have a regulatory role in biopterin biosynthesis and that patients with Parkinson's disease may have some abnormality in the regulation of biopterin biosynthesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, T -- Nagatsu, T -- Sugimoto, T -- Matsuura, S -- Kondo, T -- Iizuka, R -- Narabayashi, H -- New York, N.Y. -- Science. 1983 Jan 7;219(4580):75-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6849120" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Adrenal Glands/metabolism ; Alanine/pharmacology ; Animals ; Biopterin/*blood ; Corpus Striatum/metabolism ; Humans ; Injections, Intraperitoneal ; Liver/metabolism ; Male ; Parkinson Disease/*blood ; Pteridines/*blood ; Rats ; Rats, Inbred Strains ; Time Factors ; Tyrosine/administration & dosage/*pharmacology
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  • 18
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    Normalization of spiroperidol binding in the denervated rat striatum by homologous grafts of substantia nigra (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-11-25
    Description: Transplantation of embryonic substantia nigra into the adult rat brain decreases the motor asymmetry that is produced by dopamine receptor supersensitivity after a unilateral lesion of the substantia nigra. The authors report that this effect of transplantation is specific to grafts of substantia nigra. They also report that, in conjunction with the decrease in motor asymmetry, these grafts cause postsynaptic dopaminergic binding sites to return to normal density as measured by tritiated spiroperidol autoradiography. Thus, in animals with brain lesions, grafts of substantia nigra produce a long-term alteration in the functional status of host brain cell receptors that is associated with a reduction in the behavioral deficit.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, W J -- Ko, G N -- Niehoff, D L -- Kuhar, M J -- Hoffer, B J -- Olson, L -- Cannon-Spoor, H E -- Morihisa, J M -- Wyatt, R J -- MH-00289/MH/NIMH NIH HHS/ -- MH-25951/MH/NIMH NIH HHS/ -- NS-09199/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 Nov 25;222(4626):937-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6635666" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apomorphine/pharmacology ; Autoradiography ; Denervation ; Dextroamphetamine/pharmacology ; Motor Activity/drug effects ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/*metabolism ; Spiperone/metabolism ; Substantia Nigra/*transplantation
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  • 19
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    Phorbol ester receptors: autoradiographic identification in the developing rat (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-12-02
    Description: Autoradiography with 3H-labeled phorbol dibutyrate was used for the light microscopic detection of phorbol ester receptors in rat fetuses. In 15- and 18-day fetuses, as well as in adult rats, receptors were found to be concentrated in the central nervous system. The localization of receptors in the ventral marginal zone of the fetal neural tube, the lens of the eye, and other sites suggests a role for phorbol ester receptors in cellular process extension and cell-cell interaction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Murphy, K M -- Gould, R J -- Oster-Granite, M L -- Gearhart, J D -- Snyder, S H -- New York, N.Y. -- Science. 1983 Dec 2;222(4627):1036-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6316499" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Brain/embryology ; Brain Chemistry ; *Caenorhabditis elegans Proteins ; Carrier Proteins ; Cell Communication ; Cell Division ; Central Nervous System/analysis/*embryology ; Eye/embryology ; Fetus/*analysis ; Intestines/embryology ; Lens, Crystalline/embryology ; Phorbol 12,13-Dibutyrate ; Phorbol Esters/*metabolism ; Phorbols/*metabolism ; *Protein Kinase C ; Rats ; Rats, Inbred Strains ; Receptors, Cell Surface/*analysis ; *Receptors, Drug
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  • 20
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    Alcohol-induced spasms of cerebral blood vessels: relation to cerebrovascular accidents and sudden death (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-15
    Description: Ethyl alcohol produced graded contractile responses in rat cerebral arterioles and venules in vivo and in isolated canine basilar and middle cerebral arteries at a concentration range (10 to 500 milligrams per deciliter) which parallels that needed for its graded effects of euphoria, mental haziness, muscular incoordination, stupor, and coma in humans. Two specific calcium antagonists, nimodipine and verapamil, prevented or reversed the alcohol-induced cerebrovasospasm and thus may prove valuable in treating the hypertension and stroke observed in heavy users of alcohol.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Altura, B M -- Altura, B T -- Gebrewold, A -- DA02339/DA/NIDA NIH HHS/ -- HL29600/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):331-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836278" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cerebral Arteries/drug effects ; Cerebrovascular Circulation/drug effects ; Cerebrovascular Disorders/*chemically induced ; Death, Sudden/*etiology ; Dogs ; Ethanol/*adverse effects ; Humans ; Ischemic Attack, Transient/*chemically induced ; Male ; Rats ; Rats, Inbred Strains ; Vasoconstriction/drug effects
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  • 21
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    Endogenous pyrogen activity in human plasma after exercise (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-05-06
    Description: Plasma obtained from human subjects after exercise and injected intraperitoneally into rats elevated rat rectal temperature and depressed plasma iron and zinc concentrations. The pyrogenic component was heat-denaturable and had an apparent molecular weight of 14,000 daltons. Human mononuclear leukocytes obtained after exercise and incubated in vitro released a factor into the medium that also elevated body temperature in rats and reduced trace metal concentrations. These results suggest that endogenous pyrogen, a protein mediator of fever and trace metal metabolism during infection, is released during exercise.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cannon, J G -- Kluger, M J -- AI 13878/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1983 May 6;220(4597):617-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6836306" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Animals ; Body Temperature/drug effects ; Female ; Humans ; *Interleukin-1 ; Iron/blood ; Leukocytes/physiology ; Male ; Molecular Weight ; *Physical Exertion ; Proteins/physiology ; Pyrogens/blood/*metabolism ; Rats ; Rats, Inbred Strains ; Zinc/blood
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  • 22
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    Local cerebral blood flow increases during auditory and emotional processing in the conscious rat (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-08-05
    Description: Local cerebral blood flow was measured in rats by the 14C-labeled iodoantipyrine technique with quantitative autoradiography during the processing of environmental stimuli. Presentation of a tone increased blood flow in the auditory but not the visual pathway. When the animal had previously been conditioned to fear the tone, blood flow additionally increased in the hypothalamus and amygdala. Local cerebral blood flow can thus be used to detect patterns of cerebral excitation associated with transient (30- to 40-second) mental events in experimental animals.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉LeDoux, J E -- Thompson, M E -- Iadecola, C -- Tucker, L W -- Reis, D J -- HL 18974/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1983 Aug 5;221(4610):576-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867731" target="_blank"〉PubMed〈/a〉
    Keywords: Acoustic Stimulation ; Amygdala/blood supply ; Animals ; Autoradiography ; Brain/*blood supply/physiology ; Consciousness/physiology ; Emotions/*physiology ; Hearing/*physiology ; Hypothalamus/blood supply ; Male ; Rats ; Rats, Inbred Strains
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  • 23
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    L-tryptophan: a common denominator of biochemical and neurological events of acute hepatic porphyria? (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-12-02
    Description: Hepatic porphyrias are disorders of heme synthesis characterized by genetically determined lesions of one of the key enzymes of heme synthesis. In carriers of such lesions, several factors (drugs, environmental chemicals, or diet) precipitate acute and often fatal attacks of neurologic dysfunction, which are promptly relieved by intravenous infusion of heme. However, the mechanism of such heme-induced amelioration remains elusive. To probe this mechanism, the biochemical events triggered by acute hepatic heme deficiency were examined in an animal model of chemically induced porphyria. Acute hepatic heme depletion in porphyric rats was found to impair hepatic tryptophan pyrrolase activity which, in turn, elevated tryptophan and 5-hydroxytryptamine turnover in the brain. These alterations in porphyric rats were dramatically reversed by parenteral heme administration. These findings suggest that increased tryptophan and 5-hydroxytryptamine in the nervous system may be responsible for the neurologic dysfunctions observed in humans with acute attacks of hepatic porphyria.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Litman, D A -- Correia, M A -- AM-26506/AM/NIADDK NIH HHS/ -- AM-26743/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1983 Dec 2;222(4627):1031-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6648517" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Heme/*deficiency/pharmacology ; Liver/enzymology ; Liver Diseases/complications/*metabolism ; Male ; Nervous System Diseases/etiology ; Porphyrias/complications/*metabolism ; Rats ; Rats, Inbred Strains ; Serotonin/metabolism ; Tryptophan/*metabolism ; Tryptophan Oxygenase/metabolism
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  • 24
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    Fetal brain transplant: reduction of cognitive deficits in rats with frontal cortex lesions (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-07-29
    Description: Frontal cortex and cerebellar tissue from fetal rats was implanted into the damaged frontal cortex of adults. Cognitive deficits in spatial alternation learning that follow bilateral destruction of medial frontal cortex were reduced in rats with frontal cortex implants but not in those with implants of cerebellum. Histological evaluation showed that connections were made between the frontal cortex implants and host brain tissue.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Labbe, R -- Firl, A Jr -- Mufson, E J -- Stein, D G -- New York, N.Y. -- Science. 1983 Jul 29;221(4609):470-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6683427" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal ; Cerebellum/*transplantation ; Cerebral Cortex/injuries/*transplantation ; Cognition Disorders/*physiopathology ; Fetus/*surgery ; Humans ; Male ; Rats ; Rats, Inbred Strains
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  • 25
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    Evidence for olfactory function in utero (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-07-29
    Description: Pregnant rats received 2-[14C]deoxy-D-glucose (2DG) intravenously on the last day of gestation, and their fetuses were delivered 1 hour later by cesarean section. Fetal brains showed high 2DG uptake spread throughout the accessory olfactory bulb and little or no differential uptake in the main olfactory bulb. These findings demonstrate that functional activity occurs in the accessory olfactory bulb in utero and suggest that the accessory olfactory system may be the pathway by which fetal rats detect the odor quality of their intrauterine milieu.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedersen, P E -- Stewart, W B -- Greer, C A -- Shepherd, G M -- F32-NS06978/NS/NINDS NIH HHS/ -- NS 16993/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 29;221(4609):478-80.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6867725" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Brain/radionuclide imaging ; Deoxyglucose/metabolism ; Female ; Fetus/*physiology ; Olfactory Bulb/physiology/radionuclide imaging ; Pregnancy ; Rats ; Rats, Inbred Strains ; Smell/*physiology
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  • 26
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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
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  • 27
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    Physiological correlates of prolonged sleep deprivation in rats (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-07-08
    Description: The issue of whether sleep is physiologically necessary has been unresolved because experiments that reported deleterious effects of sleep deprivation did not control for the stimuli used to prevent sleep. In this experiment, however, experimental and control rats received the same relatively mild physical stimuli, but stimulus presentations were timed to reduce sleep severely in experimental rats but not in controls. Experimental rats suffered severe pathology and death; control rats did not.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rechtschaffen, A -- Gilliland, M A -- Bergmann, B M -- Winter, J B -- MH-18428/MH/NIMH NIH HHS/ -- MH-4151/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857280" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/pathology ; Animals ; Body Weight ; Electroencephalography ; Male ; Organ Size ; Rats ; Rats, Inbred Strains ; Sleep Deprivation/*physiology ; Time Factors
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  • 28
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    Insulin elicits ingestion in decerebrate rats (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-07-08
    Description: Insulin administered to rats reliably elicits ingestion of food. To determine whether the neural mechanisms sufficient to control insulin-elicited ingestion are located in or caudal to the forebrain, decerebrate rats were treated with insulin and ingestive responses were measured. Insulin treatment produced hypoglycemia that was comparable, in magnitude and duration, in control and decerebrate rats. Decerebrate and control rats ingested significantly more sucrose solution while hypoglycemic than while normoglycemic. In contrast, insulin did not augment the water consumption of either group. These data indicate that neural systems caudal to the forebrain are sufficient to control ingestive consummatory behavior through the integration of metabolic signals generated by insulin treatment and taste afferent input from the oropharynx.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Flynn, F W -- Grill, H J -- AM 21397/AM/NIADDK NIH HHS/ -- T32-MH15012/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):188-90.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6344221" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/analysis ; Brain/*physiology ; Decerebrate State/physiopathology ; Eating/*drug effects ; Energy Metabolism ; Insulin/*pharmacology ; Male ; Rats ; Rats, Inbred Strains ; Taste/physiology
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  • 29
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    Serum factor supporting long-term survival of rat central neurons in culture (1983)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1983-06-24
    Description: Gel filtration of serum at pH 3.6 yielded a fraction that supported long-term (months) survival of dissociated rat central neurons in monolayer culture more reliably than the traditionally used unfractionated serum. The cultures remained neuron-rich, because this fraction did not support the proliferation of glia and fibroblasts that occurs in whole serum. With an apparent molecular weight of 55,000 and an isoelectric point of 5.6, the active factor (or factors) in this fraction is distinct from any well-defined growth factor.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kaufman, L M -- Barrett, J N -- NS07044/NS/NINDS NIH HHS/ -- NS12207/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 24;220(4604):1394-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857258" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cattle ; *Cell Survival/drug effects ; Cells, Cultured ; Chromatography, Gel ; Horses ; Isoelectric Focusing ; Molecular Weight ; Nerve Growth Factors/isolation & purification/*pharmacology ; Neurons/drug effects/*physiology ; Rats ; Rats, Inbred Strains ; Spinal Cord/cytology
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  • 30
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    Trigeminal-taste interaction in palatability processing (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-10
    Description: Peripheral transection of the sensory branches of the trigeminal nerve in rats unbalanced palatability, selectively reducing the ingestive actions elicited by preferred tastes but leaving unchanged the aversive actions elicited by unpreferred tastes. The reduction in the number of positive ingestive actions occurred even though the capacity to emit these actions remained unimpaired. These findings show that there is an interaction between somatosensation and gustation in the processing of palatability.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berridge, K C -- Fentress, J C -- New York, N.Y. -- Science. 1985 May 10;228(4700):747-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3992242" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Food Preferences ; Humans ; Male ; Rats ; Rats, Inbred Strains ; Taste/*physiology ; Tongue/physiology ; Trigeminal Nerve/*physiology
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  • 31
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    Selective extraction of small and large molecules from the cerebrospinal fluid by Purkinje neurons (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-04-19
    Description: Cerebellar Purkinje neurons accumulated propidium iodide, granular blue, and horseradish peroxidase conjugated to wheat germ agglutinin but not unconjugated horseradish peroxidase, bisbenzimide, or Evans blue when these compounds were infused into the lateral cerebral ventricles of awake, unrestrained rats. Accumulation of propidium iodide by Purkinje neurons of the vermis was associated with a reproducible behavioral abnormality characterized by truncal tremor, ataxia, and nystagmus. Both the accumulation of propidium iodide in Purkinje cells and the behavioral abnormality were prevented by prior intracerebroventricular administration of ouabain or colchicine, drugs that block neuronal transport processes. The ability of cerebellar Purkinje neurons to extract small and large molecules from the cerebrospinal fluid has important implications for their physiology and pathology.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Borges, L F -- Elliott, P J -- Gill, R -- Iversen, S D -- Iversen, L L -- New York, N.Y. -- Science. 1985 Apr 19;228(4697):346-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2580350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bisbenzimidazole/metabolism ; Cerebrospinal Fluid/*physiology ; Dendrites/physiology ; Evans Blue/metabolism ; Horseradish Peroxidase/metabolism ; Humans ; Male ; Propidium/metabolism/pharmacology ; Purkinje Cells/*metabolism/physiology ; Rats ; Rats, Inbred Strains ; Tremor/chemically induced/physiopathology
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    Hormonal control of the anatomical specificity of motoneuron-to-muscle innervation in rats (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-15
    Description: Motoneurons of the spinal nucleus of the bulbocavernosus innervate bulbocavernosus muscles in male rats. Adult female rats normally lack both the spinal nucleus and its target muscles. Prenatal treatment of females with testosterone propionate resulted in adults having, like males, both the spinal nucleus and its target muscles. However, prenatal treatment with dihydrotestosterone propionate preserves the muscles but not the motoneurons. This paradoxical condition might result from (i) bulbocavernosus muscles without innervation; (ii) muscles innervated by morphologically unrecognizable motoneurons; (iii) muscles innervated by a very few spinal nucleus cells, each innervating many bulbocavernosus fibers; or (iv) muscles innervated by motoneurons outside their normal anatomical locus in the spinal nucleus. The results of retrograde marker injections into the bulbocavernosus muscles of females treated with androgen refute the first three possibilities and confirm the last: the different androgen treatments result in anatomically distinct spinal motor nuclei innervating bulbocavernosus muscles.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Breedlove, S M -- NS19790/NS/NINDS NIH HHS/ -- RR07006/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1357-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975621" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dihydrotestosterone/analogs & derivatives/pharmacology ; Female ; Male ; Motor Neurons/anatomy & histology/drug effects/*physiology ; Muscles/drug effects/*innervation ; Pregnancy ; Rats ; Rats, Inbred Strains ; Sex Differentiation/drug effects ; Testosterone/*pharmacology
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    Vitamin E reversal of the effect of extracellular calcium on chemically induced toxicity in hepatocytes (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-02-15
    Description: Isolated rat hepatocytes were incubated in the presence or absence of extracellular calcium and alpha-tocopherol succinate with three different toxic chemicals; namely, adriamycin in combination with 1,3-bis(2-chloroethyl)-1-nitrosourea, ethyl methanesulfonate, and the calcium ionophore A23187. In the absence of extracellular calcium these three compounds were far more toxic to the cells than in its presence. The addition of vitamin E to calcium-free medium, however, protected hepatocytes against toxic injury, whereas cells incubated in medium containing calcium were not protected. Hepatocyte viability during each toxic insult correlated well with the cellular alpha-tocopherol content but not with the presence or absence of extracellular calcium. These results suggest that cellular alpha-tocopherol maintains the viability of the cell during a toxic insult and that the presence or absence of vitamin E in the incubation medium probably explains the conflicting reports on the role of extracellular calcium in toxic cell death.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fariss, M W -- Pascoe, G A -- Reed, D J -- ES01978/ES/NIEHS NIH HHS/ -- ES07060/ES/NIEHS NIH HHS/ -- New York, N.Y. -- Science. 1985 Feb 15;227(4688):751-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3918345" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcimycin/toxicity ; Calcium/*physiology ; Carmustine/toxicity ; Cell Survival/*drug effects ; Cells, Cultured ; Doxorubicin/toxicity ; Ethyl Methanesulfonate/toxicity ; Liver/cytology/*drug effects ; Male ; Rats ; Rats, Inbred Strains ; Vitamin E/*physiology
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    Interaction of calcitonin and calcitonin gene-related peptide at receptor sites in target tissues (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-15
    Description: Discrete receptor sites for calcitonin (CT) and calcitonin gene-related peptide (CGRP) were found in the nervous system and in peripheral tissues. Each peptide was capable of cross-reacting with the specific receptor of the other. In contrast to CT receptors, CGRP receptors were not linked to adenylate cyclase. However, CGRP could stimulate adenylate cyclase in CT target tissues apparently by interacting with CT receptors. The relative abilities of CGRP and mammalian CT to inhibit CT binding suggest that CGRP could serve as an endogenous ligand for CT receptors in the central nervous system.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goltzman, D -- Mitchell, J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1343-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2983422" target="_blank"〉PubMed〈/a〉
    Keywords: Adenylyl Cyclases/metabolism ; Adrenal Glands/metabolism ; Animals ; Bone and Bones/metabolism ; Brain/metabolism ; Calcitonin/*metabolism ; Calcitonin Gene-Related Peptide ; Kidney/metabolism ; Male ; Nerve Tissue Proteins/*metabolism ; Pituitary Gland/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Calcitonin ; Receptors, Cell Surface/*metabolism ; Spinal Cord/metabolism
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    Choline acetyltransferase activity in striatum of neonatal rats increased by nerve growth factor (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-19
    Description: Some neurodegenerative disorders may be caused by abnormal synthesis or utilization of trophic molecules required to support neuronal survival. A test of this hypothesis requires that trophic agents specific for the affected neurons be identified. Cholinergic neurons in the corpus striatum of neonatal rats were found to respond to intracerebroventricular administration of nerve growth factor with prominent, dose-dependent, selective increases in choline acetyltransferase activity. Cholinergic neurons in the basal forebrain also respond to nerve growth factor in this way. These actions of nerve growth factor may indicate its involvement in the normal function of forebrain cholinergic neurons as well as in neurodegenerative disorders involving such cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mobley, W C -- Rutkowski, J L -- Tennekoon, G I -- Buchanan, K -- Johnston, M V -- ES07094/ES/NIEHS NIH HHS/ -- NS00603/NS/NINDS NIH HHS/ -- NS17642/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 19;229(4710):284-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2861660" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholine/physiology ; Alzheimer Disease/metabolism ; Animals ; Animals, Newborn/metabolism ; Brain/drug effects/enzymology ; Choline O-Acetyltransferase/*metabolism ; Corpus Striatum/cytology/drug effects/*enzymology ; Dose-Response Relationship, Drug ; Glutamate Decarboxylase/metabolism ; Humans ; Huntington Disease/metabolism ; Nerve Growth Factors/*pharmacology/physiology ; Neurons/enzymology/physiology ; Rats ; Rats, Inbred Strains ; Tyrosine 3-Monooxygenase/metabolism
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    A strong influence of serotonin axons on beta-adrenergic receptors in rat brain (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: The role of serotonin axons in modulating the norepinephrine neurotransmission system in rat brain was investigated. Selective lesions of the forebrain serotonergic system were made by injecting 5,7-dihydroxytryptamine into the midbrain raphe nuclei. Four to six weeks after the lesion, the uptake of 3H-labeled serotonin in the frontal cortex and the hippocampus was reduced by more than 90 percent, while neither the uptake of 3H-labeled norepinephrine nor the content of norepinephrine was affected in either tissue. The number of beta-adrenergic receptors, as measured by radioligand binding with 3H-labeled dihydroalprenolol, was increased in the frontal cortex and hippocampus of rats with lesions. Similarly, specific lesions of central serotonin axons produced by systemically administered p-chloramphetamine resulted in an increase in the binding of 3H-labeled dihydroalprenolol to beta-adrenergic receptors and in the production of adenosine 3',5'-monophosphate in response to isoproterenol. These results indicate that serotonin axons may regulate beta-adrenergic receptor number and function in brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Stockmeier, C A -- Martino, A M -- Kellar, K J -- MH08982/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996132" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/*physiology ; Cerebral Cortex/*metabolism ; Clonidine/analogs & derivatives/metabolism ; Dihydroalprenolol/metabolism ; Hippocampus/*metabolism ; Kinetics ; Male ; Norepinephrine/metabolism ; Prazosin/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic, beta/*metabolism ; Serotonin/*physiology
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    Endogenous anticonvulsant substance in rat cerebrospinal fluid after a generalized seizure (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-05-31
    Description: Cerebrospinal fluid taken from rats subjected to electroshock-induced seizures and injected into the cerebral ventricles of rats that had not been shocked increased the seizure threshold of the recipients. The anticonvulsant activity of the donor cerebrospinal fluid was antagonized by opioid antagonists and enhanced by peptidase inhibitors. These results suggest the existence of an endogenous anticonvulsant substance in rat cerebrospinal fluid, possibly opioid in nature, which is activated as a consequence of a seizure and which may play a critical role in postseizure inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tortella, F C -- Long, J B -- New York, N.Y. -- Science. 1985 May 31;228(4703):1106-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2986292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anticonvulsants/*cerebrospinal fluid ; Electroshock ; Enkephalin, Leucine/analogs & derivatives/pharmacology ; Male ; Naloxone/pharmacology ; Narcotic Antagonists/pharmacology ; Peptide Hydrolases ; Rats ; Rats, Inbred Strains ; Receptors, Opioid/drug effects ; Receptors, Opioid, delta ; Seizures/*cerebrospinal fluid
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    Hypoglycemia-induced neuronal damage prevented by an N-methyl-D-aspartate antagonist (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-11-08
    Description: The possibility that neuronal damage due to hypoglycemia is induced by agonists acting on the N-methyl-D-aspartate (NMDA) receptor was investigated in the rat caudate nucleus. Local injections of an NMDA receptor antagonist, 2-amino-7-phosphonoheptanoic acid, were performed before induction of 30 minutes of reversible, insulin-induced, hypoglycemic coma. Neuronal necrosis in these animals after 1 week of recovery was reduced 90 percent compared to that in saline-injected animals. The results suggest that hypoglycemic neuronal damage is induced by NMDA receptor agonists, such as the excitatory amino acids or related compounds.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wieloch, T -- New York, N.Y. -- Science. 1985 Nov 8;230(4726):681-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2996146" target="_blank"〉PubMed〈/a〉
    Keywords: *2-Amino-5-phosphonovalerate/*analogs & derivatives ; Amino Acids/*pharmacology ; Animals ; Aspartic Acid/*analogs & derivatives/antagonists & inhibitors ; Caudate Nucleus/cytology ; Electroencephalography ; Hypoglycemia/*metabolism/pathology ; Male ; N-Methylaspartate ; Necrosis ; Neurons/*drug effects/metabolism/pathology ; Rats ; Rats, Inbred Strains ; Receptors, N-Methyl-D-Aspartate ; Receptors, Neurotransmitter/metabolism
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    Regional myocardial substrate uptake in hypertensive rats: a quantitative autoradiographic measurement (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-22
    Description: Severe hypertension causes global and regional changes in myocardial perfusion and substrate utilization. Regional perfusion and fatty acid utilization were evaluated by dual-tracer autoradiography in normotensive and hypertensive rats of the Dahl strain. The regional distributions of perfusion and fatty acid utilization were homogeneous in normotensive rats. Severe hypertension was associated with a homogeneous pattern of regional perfusion, but fatty acid utilization was focally decreased in the free wall of the left ventricle. The decrease in fatty acid uptake was associated with a concomitant increase in glucose utilization. These findings suggest that severe hypertension is associated with uniform myocardial perfusion and focal alterations in the substrates used for the performance of myocardial work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yonekura, Y -- Brill, A B -- Som, P -- Yamamoto, K -- Srivastava, S C -- Iwai, J -- Elmaleh, D R -- Livni, E -- Strauss, H W -- Goodman, M M -- HL29636/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1494-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975623" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autoradiography ; Deoxyglucose/analogs & derivatives/metabolism ; Endocardium/metabolism ; Fatty Acids/*metabolism ; Fluorodeoxyglucose F18 ; Glucose/*metabolism ; Heart Septum/metabolism ; Hypertension/*metabolism ; Myocardium/*metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred Strains ; Tissue Distribution
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    Distribution of enkephalin immunoreactivity in germinative cells of developing rat cerebellum (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-01
    Description: The cellular distribution of enkephalin, an endogenous opioid, in the developing rat cerebellum was determined by immunocytochemistry. Methionine and leucine enkephalin were concentrated in the external germinal layer, a matrix of proliferative cells; staining was confined to the cortical cytoplasm. Enkephalin was not detected by immunocytochemistry in differentiated neural cells. These results indicate that endogenous opioids are involved specifically in early phases of nervous system development, particularly cell proliferation and differentiation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zagon, I S -- Rhodes, R E -- McLaughlin, P J -- NS-20500/NS/NINDS NIH HHS/ -- NS-20623/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1049-51.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3883485" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation ; Cell Division ; Cerebellum/cytology/*growth & development/physiology ; Enkephalin, Leucine/immunology/physiology ; Enkephalin, Methionine/immunology/physiology ; Enkephalins/immunology/*physiology ; Fluorescent Antibody Technique ; Rats ; Rats, Inbred Strains
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  • 41
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    Plasticity of hippocampal circuitry in Alzheimer's disease (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-12-06
    Description: Two markers of neuronal plasticity were used to compare the response of the human central nervous system to neuronal loss resulting from Alzheimer's disease with the response of rats to a similar neuronal loss induced by lesions. In rats that had received lesions of the entorhinal cortex, axon sprouting of commissural and associational fibers into the denervated molecular layer of the dentate gyrus was paralleled by a spread in the distribution of tritiated kainic acid-binding sites. A similar expansion of kainic acid receptor distribution was observed in hippocampal samples obtained postmortem from patients with Alzheimer's disease. An enhancement of acetylcholinesterase activity in the dentate gyrus molecular layer, indicative of septal afferent sprouting, was also observed in those patients with a minimal loss of cholinergic neurons. These results are evidence that the central nervous system is capable of a plastic response in Alzheimer's disease. Adaptive growth responses occur along with the degenerative events.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Geddes, J W -- Monaghan, D T -- Cotman, C W -- Lott, I T -- Kim, R C -- Chui, H C -- AG00538/AG/NIA NIH HHS/ -- MH 19691/MH/NIMH NIH HHS/ -- P50AG5142/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1985 Dec 6;230(4730):1179-81.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4071042" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Alzheimer Disease/*pathology ; Animals ; Hippocampus/enzymology/*pathology ; Humans ; Kainic Acid/metabolism ; Male ; *Neuronal Plasticity ; Neurons/pathology ; Rats ; Rats, Inbred Strains
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  • 42
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    Effect of vanadate on elevated blood glucose and depressed cardiac performance of diabetic rats (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-22
    Description: The trace element vanadium has an unclear biological function. Vanadate, an oxidized form of vanadium, appears to have an insulin-like action. The effect of vanadate on blood glucose and cardiac performance was assessed in female Wistar rats 6 weeks after they were made diabetic with streptozotocin. When vanadate was administered for a 4-week period to the diabetic rats, their blood glucose was not significantly different from that of nondiabetic controls despite a low serum insulin. In contrast, blood glucose was increased about threefold in the diabetic rats that were not treated with vanadate; these rats also had low insulin levels. Cardiac performance was depressed in the untreated diabetic animals, but the cardiac performance of the vanadate-treated diabetic animals was not significantly different from that of nondiabetic controls. Thus vanadate controlled the high blood glucose and prevented the decline in cardiac performance due to diabetes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Heyliger, C E -- Tahiliani, A G -- McNeill, J H -- New York, N.Y. -- Science. 1985 Mar 22;227(4693):1474-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3156405" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Glucose/*analysis ; Calcium-Transporting ATPases/antagonists & inhibitors ; Diabetes Mellitus, Experimental/blood/*physiopathology ; Drinking ; Female ; Insulin/blood ; Myocardial Contraction/*drug effects ; Myocardium/enzymology ; Rats ; Rats, Inbred Strains ; Sarcoplasmic Reticulum/enzymology ; Vanadates ; Vanadium/*pharmacology
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  • 43
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    Platelet-mediated cholesterol accumulation in cultured aortic smooth muscle cells (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-08
    Description: Cholesterol accumulates within smooth muscle cells and macrophages in atherosclerotic lesions, thereby contributing to the progressive enlargement of these lesions. The mechanism of this cellular accumulation of cholesterol is not known. The possibility that platelets may have a role in the cellular cholesterol accumulation that occurs during atherogenesis was investigated. Incubation of thrombin-activated washed rat platelets (or platelet-free supernatants prepared from thrombin-activated platelets) with cultured rat aortic smooth muscle cells induced cholesteryl ester lipid droplet accumulation within the smooth muscle cells. No cholesteryl ester lipid droplets accumulated when smooth muscle cells were incubated with unactivated platelets. Smooth muscle cell lipid droplet accumulation occurred in the absence of serum lipoproteins and was not inhibited by mevinolin, a drug that blocks cholesterol synthesis. These findings suggest that activated platelets may release cholesterol, which can be accumulated by cells and stored as lipid droplets.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kruth, H S -- New York, N.Y. -- Science. 1985 Mar 8;227(4691):1243-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975612" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta/physiopathology ; Arteriosclerosis/*physiopathology ; Blood Platelets/*physiology ; Cells, Cultured ; Cholesterol/*physiology ; Male ; Muscle, Smooth, Vascular/*cytology/physiopathology ; Platelet Aggregation ; Rats ; Rats, Inbred Strains ; Thrombin/physiology
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  • 44
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    Reexamination of glucose-6-phosphatase activity in the brain in vivo: no evidence for a futile cycle (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-07-05
    Description: Glucose-6-phosphatase activity in the rat brain in vivo was estimated by measuring the differential loss of tritium and carbon-14 from the glucose pool labeled by a mixture of [2-3H]glucose and [U-14C]glucose. The results provide no evidence of significant dephosphorylation of glucose-6-phosphate and do not support the hypothesis of a futile cycle involving glucose-6-phosphatase activity in the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nelson, T -- Lucignani, G -- Atlas, S -- Crane, A M -- Dienel, G A -- Sokoloff, L -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):60-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990038" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Glucose/metabolism ; Glucose-6-Phosphatase/*metabolism ; Glucosephosphates/*metabolism ; Glycolysis ; Male ; Rats ; Rats, Inbred Strains
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    Blood-brain barrier: endogenous modulation by adrenal-cortical function (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-29
    Description: The blood-brain barrier restricts the passage of molecules from the blood to the brain. The permeability of the barrier to iodine-125-labeled bovine serum albumin was examined in rats that had undergone adrenalectomy, adrenal demedullation, and corticosterone replacement. Adrenalectomy, but not adrenal demedullation, increased the permeability of brain tissue to the isotopically labeled macromolecule; corticosterone replacement reversed this effect. These results indicate that the blood-brain barrier may be hormonally regulated; that is, the pituitary-adrenal axis may physiologically modulate the permeability of the brain microvasculature to macromolecules.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Long, J B -- Holaday, J W -- New York, N.Y. -- Science. 1985 Mar 29;227(4694):1580-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975627" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/*physiology ; Adrenal Medulla/physiology ; Adrenalectomy ; Animals ; Blood Pressure ; *Blood-Brain Barrier ; Central Nervous System/physiology ; Corticosterone/blood/physiology ; Male ; Pituitary-Adrenal System/physiology ; Rats ; Rats, Inbred Strains ; Serum Albumin, Bovine/metabolism
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  • 46
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    Ascorbic acid and the behavioral response to haloperidol: implications for the action of antipsychotic drugs (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-01-25
    Description: Haloperidol, a widely used antipsychotic drug, was tested for its ability to block the behavioral response to amphetamine and to elicit catalepsy in rats treated with saline or ascorbic acid (1000 milligrams per kilogram of body weight). By itself, ascorbic acid failed to exert significant behavioral effects, but it enhanced the antiamphetamine and cataleptogenic effects of haloperidol (0.1 or 0.5 milligrams per kilogram). These results, combined with a growing body of biochemical evidence, suggest that ascorbic acid plays an important role in modulating the behavioral effects of haloperidol and related antipsychotic drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rebec, G V -- Centore, J M -- White, L K -- Alloway, K D -- DA 02451/DA/NIDA NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 25;227(4685):438-40.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4038426" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascorbic Acid/*pharmacology ; Behavior, Animal/*drug effects ; Catalepsy/chemically induced ; Dextroamphetamine/pharmacology ; Drug Synergism ; Haloperidol/*pharmacology ; Humans ; Male ; Motor Activity/drug effects ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/metabolism
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  • 47
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    Glucocorticoids potentiate ischemic injury to neurons: therapeutic implications (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-09-27
    Description: Sustained exposure to glucocorticoids, the adrenocortical stress hormones, is toxic to neurons, and such toxicity appears to play a role in neuron loss during aging. Previous work has shown that glucocorticoids compromise the capacity of neurons to survive a variety of metabolic insults. This report extends those observations by showing that ischemic injury to neurons in rat brain is also potentiated by exposure to high physiological titers of glucocorticoids and is attenuated by adrenalectomy. The synergy between ischemic and glucocorticoid brain injury was seen even when glucocorticoid levels were manipulated after the ischemic insult. Pharmacological interventions that diminish the adrenocortical stress response may improve neurological outcome from stroke or cardiac arrest.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R M -- Pulsinelli, W A -- NS-03346/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Sep 27;229(4720):1397-400.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4035356" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenalectomy ; Animals ; Brain/cytology/drug effects ; Brain Ischemia/metabolism/*physiopathology ; Cerebral Cortex/drug effects ; Cerebrovascular Disorders/physiopathology ; Corpus Striatum/drug effects ; Glucocorticoids/*pharmacology ; Heart Arrest/physiopathology ; Hippocampus/drug effects ; Humans ; Male ; Neurons/*drug effects ; Rats ; Rats, Inbred Strains
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  • 48
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    Monitoring the time course of cerebral deoxyglucose metabolism by 31P nuclear magnetic resonance spectroscopy (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-06-14
    Description: The phosphorylation of 2-deoxyglucose by the mammalian brain is used as an index of the brain's energy metabolism. The results of phosphorus-31 nuclear magnetic resonance (31P NMR) monitoring of conscious animals in vivo showed rapid phosphorylation of 2-deoxyglucose by brain tissue. The rate of phosphorylation as determined by 31P NMR was consistent with results achieved by tracer methods using carbon-14-labeled 2-deoxyglucose. However, the disappearance of 2-deoxyglucose-6-phosphate was shown to be faster than that reported by tracer studies and occurred without alterations of intracellular pH and energy homeostasis. These results were confirmed by gas chromatography and mass spectroscopy. It is postulated that 2-deoxyglucose may be metabolized in several ways, including dephosphorylation by a hexose phosphatase.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Deuel, R K -- Yue, G M -- Sherman, W R -- Schickner, D J -- Ackerman, J J -- AM-20579/AM/NIADDK NIH HHS/ -- GM-30331/GM/NIGMS NIH HHS/ -- RR 00954/RR/NCRR NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jun 14;228(4705):1329-31.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4001946" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*metabolism ; Deoxy Sugars/*metabolism ; Deoxyglucose/*metabolism ; Kinetics ; Magnetic Resonance Spectroscopy ; Phosphorylation ; Rats ; Rats, Inbred Strains
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  • 49
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    Regional brain dopamine metabolism: a marker for the speed, direction, and posture of moving animals (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-05
    Description: Brain dopamine is necessary for normal movement. To determine whether there is a precise relation between the intensity of movement and changes in brain dopamine metabolism, the investigators ran rats on straight and circular treadmills at different speeds and with different body postures. Concentrations of dopamine and its metabolite 3,4-dihydroxyphenylacetic acid increased in the caudate and accumbens nuclei in direct relation to the speed and angular posture of the animals. Dopamine metabolism in the nucleus accumbens was more strongly linked to the speed and direction of movement, while in the caudate nucleus dopamine and 3,4-dihydroxyphenylacetic acid were affected most by posture and direction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Freed, C R -- Yamamoto, B K -- K04-HL 00782/HL/NHLBI NIH HHS/ -- P50 NS 09199/NS/NINDS NIH HHS/ -- R01 NS 18639/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Jul 5;229(4708):62-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4012312" target="_blank"〉PubMed〈/a〉
    Keywords: 3,4-Dihydroxyphenylacetic Acid/metabolism ; Animals ; Brain/*metabolism ; Caudate Nucleus/metabolism ; Dopamine/*metabolism ; Male ; *Motor Activity ; Nucleus Accumbens/metabolism ; *Posture ; Rats ; Rats, Inbred Strains
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  • 50
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    A specific 37,000-dalton protein that accumulates in regenerating but not in nonregenerating mammalian nerves (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-04-26
    Description: A 37-kilodalton protein is synthesized at higher rates in the peripheral and central nervous system of newborn rats than in adult animals. As a specific response to denervation, the synthesis of the 37-kilodalton protein is increased in the mature peripheral and central nervous system; however, this protein accumulates only in the peripheral nervous system. The differences in accumulation of the protein correlate with the apparent differences in the ability of peripheral and central axons to regenerate. The synthesis of the 37-kilodalton protein is inhibited when proper innervation or reinnervation is established.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Muller, H W -- Gebicke-Harter, P J -- Hangen, D H -- Shooter, E M -- NS 04270/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1985 Apr 26;228(4698):499-501.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3983637" target="_blank"〉PubMed〈/a〉
    Keywords: Aging ; Animals ; Animals, Newborn/physiology ; Axons/physiology ; Brain/physiology ; Central Nervous System/metabolism/*physiology ; Molecular Weight ; *Nerve Regeneration ; Nerve Tissue Proteins/*biosynthesis ; Optic Nerve/physiology ; Peripheral Nerves/metabolism/*physiology ; Photofluorography ; Rats ; Rats, Inbred Strains ; Sciatic Nerve/physiology ; Spinal Cord/physiology
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  • 51
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    Patterns of growth hormone-releasing factor and somatostatin secretion into the hypophysial-portal circulation of the rat (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-25
    Description: The interrelation between the secretion of two hypophysiotropic peptides, growth hormone-releasing factor (GRF) and somatostatin (SRIF), in the generation of episodic growth hormone (GH) secretion was inferred from direct measurements of immunoreactive GRF and immunoreactive SRIF concentrations in the hypophysial-portal plasma of the rat. Secretion of immunoreactive GRF was found to be episodic, with maximal concentrations present during periods of expected GH secretory episodes. Secretion of immunoreactive GRF was accompanied by a moderate reduction in portal plasma levels of immunoreactive SRIF. Passive immunoneutralization of SRIF was associated with increased concentrations of immunoreactive GRF in hypophysial-portal plasma. On the basis of these observations, it appears that each GH secretory episode is initiated by pulsatile secretion of immunoreactive GRF into the portal circulation, which is preceded by or is concurrent with a moderate reduction of inhibitory tone provided by portal immunoreactive SRIF. These experiments provide direct insights into central and adenohypophysial mechanisms by which GRF and SRIF interact to generate episodic secretion of GH.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Plotsky, P M -- Vale, W -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1985 Oct 25;230(4724):461-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2864742" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Hormone/blood/physiology/secretion ; Growth Hormone-Releasing Hormone/blood/physiology/*secretion ; Immune Sera/immunology ; Male ; Pituitary Gland/blood supply/*physiology ; Pituitary Gland, Anterior/secretion ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; Sheep/immunology ; Somatostatin/blood/physiology/*secretion
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  • 52
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    Vasopressin-stimulated release of atriopeptin: endocrine antagonists in fluid homeostasis (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-07-26
    Description: Administration of pharmacological doses of arginine-vasopressin, related peptides, and other pressor agents induced a profound release of atriopeptin immunoreactivity into the circulation. The stimulated release of atriopeptin apparently was related to increased arterial blood pressure. Neither the nonpressor vasopressin analog 1-deamino-D-Arg8-vasopressin nor arginine-vasopressin in the presence of a specific pressor antagonist caused atriopeptin to be released into the circulation. Urine output was correlated with the level of atriopeptin released. Physiological levels of arginine-vasopressin suppress diuresis and produced vasoconstriction. Pharmacological levels of the hormone stimulated the cardiac endocrine system to release atriopeptin, which may cause diuresis and vasodilation to physiologically antagonize the effects of vasopressin.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Manning, P T -- Schwartz, D -- Katsube, N C -- Holmberg, S W -- Needleman, P -- New York, N.Y. -- Science. 1985 Jul 26;229(4711):395-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2990050" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/pharmacology ; Angiotensin II/pharmacology ; Animals ; Arginine Vasopressin/*pharmacology ; *Atrial Function ; Blood Pressure/drug effects ; Deamino Arginine Vasopressin/pharmacology ; Dose-Response Relationship, Drug ; Male ; Muscle Proteins/*secretion ; Oxytocin/pharmacology ; Phenylephrine/pharmacology ; Rats ; Rats, Inbred Strains ; Urodynamics/drug effects ; Water-Electrolyte Balance/*drug effects
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  • 53
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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)
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    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
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  • 54
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    Methionine and leucine enkephalin in rat neurohypophysis: different responses to osmotic stimuli and T2 toxin (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-05-03
    Description: Specific radioimmunoassays were used to measure the effects of hypertonic saline (salt loading), water deprivation, and trichothecene mycotoxin (T2 toxin) on the content of methionine enkephalin (ME), leucine enkephalin (LE), alpha-neoendorphin, dynorphin A, dynorphin B, vasopressin, and oxytocin in the rat posterior pituitary. Concentrations of vasopressin and oxytocin decreased in response to both osmotic stimuli and treatment with T2 toxin, but the decrease was greater with osmotic stimulations. Similarly, concentrations of LE and dynorphin-related peptides declined after salt loading and water deprivation; LE concentrations also decreased after treatment with T2 toxin. The concentration of ME decreased after water deprivation, did not change after salt loading, and increased after T2 toxin treatment. The differentiating effects of these stimuli on the content of immunoreactive LE and ME are consistent with the hypothesis that LE and ME may be localized in separate populations of nerve endings with different roles in the posterior pituitary.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zamir, N -- Zamir, D -- Eiden, L E -- Palkovits, M -- Brownstein, M J -- Eskay, R L -- Weber, E -- Faden, A I -- Feuerstein, G -- New York, N.Y. -- Science. 1985 May 3;228(4699):606-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858918" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Dynorphins/analogs & derivatives/analysis ; Endorphins/analysis ; Enkephalin, Leucine/*analysis ; Enkephalin, Methionine/*analysis ; Male ; Osmosis ; Oxytocin/analysis ; Pituitary Gland, Posterior/*analysis/drug effects ; Protein Precursors/analysis ; Rats ; Rats, Inbred Strains ; Saline Solution, Hypertonic ; Sesquiterpenes/*pharmacology ; T-2 Toxin/*pharmacology ; Vasopressins/analysis ; Water Deprivation
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    Leukotrienes as mediators in tissue trauma (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-10-18
    Description: A significant increase in the production of cysteinyl leukotrienes was observed after mechanical or thermal trauma in the anesthesized rat. The amount of biliary N-acetyl-leukotriene E4, which represents a suitable indicator for blood plasma leukotrienes, was used as a measure of leukotriene generation. Cysteinyl leukotrienes were rapidly eliminated from blood plasma into bile where N-acetyl-leukotriene E4 was the major metabolite. Leukotrienes were at a much lower concentration in blood plasma than in bile and differed in the pattern of metabolites. The detected amounts of leukotrienes were sufficient to induce known phenomena associated with trauma, such as tissue edema and circulatory and respiratory dysfunction. Increased leukotriene generation appears to play an important role in the pathophysiology of tissue trauma.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Denzlinger, C -- Rapp, S -- Hagmann, W -- Keppler, D -- New York, N.Y. -- Science. 1985 Oct 18;230(4723):330-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/4048937" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Abdominal/injuries ; Bile/metabolism ; Bile Ducts/surgery ; Burns/physiopathology ; Female ; Fractures, Bone/physiopathology ; Half-Life ; Kinetics ; Rats ; Rats, Inbred Strains ; SRS-A/*biosynthesis/blood ; Tritium ; Wounds and Injuries/*physiopathology
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  • 56
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    Targeted modulation of acute inflammation (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-01-11
    Description: Localized inflammation of the lungs was induced with the neutrophil chemoattractant, N-formylmethionylleucylphenylalanine (FMLP) in combination with magnetically responsive albumin microspheres, a drug carrier that provides efficient, extremely rapid localization in tissue. Intravenous targeting to rat lungs was accomplished by means of an external thoracic magnet. This caused progressive local accumulation of neutrophils, extravascular cell migration, and acute tissue injury. Microscopic findings favored chemotaxis as the principal mechanism of cell accumulation. This system provides a new experimental model for acute alveolar damage, a rapid in vivo assay for drugs that modulate neutrophil chemotaxis, and a new therapeutic approach to focusing inflammation in patients with chemotactic defects.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ranney, D F -- CA15673/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1985 Jan 11;227(4683):182-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3966151" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Chemotaxis, Leukocyte ; Disease Models, Animal ; Magnetics ; Microspheres ; N-Formylmethionine Leucyl-Phenylalanine/*pharmacology ; Pneumonia/*etiology/immunology ; Pulmonary Edema/etiology/immunology ; Rats ; Rats, Inbred Strains ; Serum Albumin
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  • 57
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    Abrupt induction of a membrane digestive enzyme by its intraintestinal substrate (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-01-04
    Description: The regulation of amino-oligopeptidase (AOP), an intestinal brush border hydrolase essential for the surface digestion of peptide nutrients, was examined in rats in vivo. Short-term (30-minute) intraintestinal perfusion of a tetrapeptide substrate, Gly-Leu-Gly-Gly, or a synthetic substrate, leucyl-beta-naphthylamide, induced a doubling in the incorporation of [3H]leucine into the AOP in association with intracellular membranes. The subsequent conversion of AOP from nascent to mature enzyme and its membrane-associated transport to the brush border occurred at normal rates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Reisenauer, A M -- Gray, G M -- AM 07056/AM/NIADDK NIH HHS/ -- AM 11270/AM/NIADDK NIH HHS/ -- AM 15802/AM/NIADDK NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1985 Jan 4;227(4682):70-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3838079" target="_blank"〉PubMed〈/a〉
    Keywords: Aminopeptidases/*biosynthesis ; Animals ; *Antigens, CD13 ; Dietary Proteins/metabolism ; Digestion ; Endoplasmic Reticulum/metabolism ; Enzyme Induction ; Golgi Apparatus/metabolism ; Intestines/*enzymology ; Kinetics ; Leucine/analogs & derivatives/metabolism ; Male ; Microvilli/enzymology ; Oligopeptides/metabolism ; Rats ; Rats, Inbred Strains
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  • 58
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    Response to ethanol reduced by past thiamine deficiency (1985)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 1985-03-15
    Description: Ethanol-induced intoxication and hypothermia were studied in rats approximately 7 months after severe thiamine deficiency, when treated rats appeared to have recovered their physical health. Previously induced thiamine deficiency without prior ethanol exposure significantly decreased the area under the curve plotted for the concentration of ethanol in blood and also decreased behavioral impairment and hypothermia due to ethanol exposure. Pathophysiologic changes resulting from thiamine deficiency may contribute to both the pharmacodynamic and pharmacokinetic tolerance to ethanol in chronic alcoholics.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Martin, P R -- Majchrowicz, E -- Tamborska, E -- Marietta, C -- Mukherjee, A B -- Eckardt, M J -- New York, N.Y. -- Science. 1985 Mar 15;227(4692):1365-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3975622" target="_blank"〉PubMed〈/a〉
    Keywords: Alcohol Amnestic Disorder/pathology ; Alcoholic Intoxication/physiopathology ; Animals ; Behavior, Animal/drug effects ; Body Temperature/drug effects ; Brain/pathology ; Ethanol/*pharmacology ; Female ; Humans ; Hypothermia/chemically induced ; Male ; Rats ; Rats, Inbred Strains ; Thiamine Deficiency/*physiopathology ; Wernicke Encephalopathy/pathology
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  • 59
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    Antigenic and genetic properties of viruses linked to hemorrhagic fever with renal syndrome (1985)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1985-03-01
    Description: Hemorrhagic fever with renal syndrome (HFRS) comprises a variety of clinically similar diseases of viral etiology that are endemic to and sporadically epidemic throughout the Eurasian continent and Japan. Although HFRS has not been reported in North America, viruses that are antigenically similar to HFRS agents were recently isolated from rodents in the United States. Examination and comparison of eight representative isolates from endemic disease areas and from regions with no known associated HFRS indicate that these viruses represent a new and unique group that constitutes a separate genus in the Bunyaviridae family of animal viruses.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schmaljohn, C S -- Hasty, S E -- Dalrymple, J M -- LeDuc, J W -- Lee, H W -- von Bonsdorff, C H -- Brummer-Korvenkontio, M -- Vaheri, A -- Tsai, T F -- Regnery, H L -- New York, N.Y. -- Science. 1985 Mar 1;227(4690):1041-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2858126" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Viral/immunology ; Arvicolinae ; Base Sequence ; Bunyaviridae/genetics ; Hantavirus/genetics/*immunology ; Hemorrhagic Fever with Renal Syndrome/genetics/immunology/*microbiology ; Humans ; Korea ; Mice ; Muridae ; Neutralization Tests ; RNA Viruses/*immunology ; Radioimmunoassay ; Rats ; Rats, Inbred Strains ; United States
    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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  • 60
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    Ionizing radiation decreases veratridine-stimulated uptake of sodium in rat brain synaptosomes (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-03
    Description: Veratridine-stimulated uptake of sodium-22 in brain synaptosomes was significantly reduced by ionizing radiation over a dose range of 10 to 1000 rads. The response was dose-dependent and involved a decrease in the maximum effect of veratridine on uptake. The central nervous system may be more sensitive to ionizing radiation than generally thought, perhaps through a loss of the ability of the sodium channel to respond properly to stimulation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wixon, H N -- Hunt, W A -- New York, N.Y. -- Science. 1983 Jun 3;220(4601):1073-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302846" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/drug effects/*radiation effects ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Ion Channels/drug effects/radiation effects ; Male ; Rats ; Rats, Inbred Strains ; Sodium/*metabolism ; Synaptosomes/drug effects/*radiation effects ; Veratridine/*pharmacology ; Veratrine/*analogs & derivatives
    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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  • 61
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    High fetal estrogen concentrations: correlation with increased adult sexual activity and decreased aggression in male mice (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-06-17
    Description: In the house mouse (Mus musculus), fetuses may develop in utero next to siblings of the same or opposite sex. The amniotic fluid of the female fetuses contains higher concentrations of estradiol than that of male fetuses. Male fetuses that developed in utero between female fetuses had higher concentrations of estradiol in their amniotic fluid than males that were located between other male fetuses during intrauterine development. They were also more sexually active as adults, less aggressive, and had smaller seminal vesicles than males that had developed between other male fetuses in utero. These findings raise the possibility that during fetal life circulating estrogens may interact with circulating androgens both in regulating the development of sex differences between males and females and in producing variation in phenotype among males and among females.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉vom Saal, F S -- Grant, W M -- McMullen, C W -- Laves, K S -- MH35079/MH/NIMH NIH HHS/ -- RR07053/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 1983 Jun 17;220(4603):1306-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857252" target="_blank"〉PubMed〈/a〉
    Keywords: Aggression/*drug effects ; Amniotic Fluid/analysis ; Animals ; Estradiol/analysis/*pharmacology/physiology ; Female ; Fetus/*drug effects/physiology ; Humans ; Male ; Mice ; Progesterone/pharmacology ; Rats ; Rats, Inbred Strains ; Sex Differentiation/drug effects ; Sexual Behavior, Animal/*drug effects/physiology ; Testosterone/analysis/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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  • 62
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    Spontaneous orofacial dyskinesia and dopaminergic function in rats after 6 months of neuroleptic treatment (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-04-29
    Description: A syndrome of spontaneous orofacial dyskinesia was identified in groups of rats treated for 6 months with a wide range of neuroleptic drugs. Phenothiazines, thioxanthenes, and substituted benzamides were particularly likely to induce the syndrome. It was observed in the presence of a functional blockade of dopamine receptors and endured for at least 2.5 months after drug withdrawal. There was no relation between the syndrome and changes in striatal dopamine receptors, as indexed by the binding of tritiated spiperone and tritiated cis(Z)-flupenthixol. The syndrome parallels several of the features of clinical tardive dyskinesia, whose pathophysiology thus may not involve changes in the characteristics of striatal dopamine receptors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Waddington, J L -- Cross, A J -- Gamble, S J -- Bourne, R C -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):530-2.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6132447" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Animals ; Antipsychotic Agents/*adverse effects ; Dyskinesia, Drug-Induced/*etiology ; Fluphenazine/administration & dosage/adverse effects/analogs & derivatives ; Haloperidol/adverse effects/pharmacology ; Humans ; Injections, Intramuscular ; Male ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/*drug effects/physiology
    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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  • 63
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    Differential effects of classical and atypical antipsychotic drugs on A9 and A10 dopamine neurons (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-09-09
    Description: Prolonged treatment with classical antipsychotic drugs decreased the number of spontaneously active dopamine neurons in both the substantia nigra (A9) and the ventral tegmental area (A10) of the rat brain. In contrast, treatment with atypical antipsychotic drugs selectively decreased the number of A10 dopamine neurons. Related drugs lacking antipsychotic efficacy failed to decrease dopamine activity. These findings suggest that the inability of atypical antipsychotic drugs to decrease A9 dopamine neuronal activity may be related to their lower potential for causing tardive dyskinesia and that the inactivation of A10 neurons may be involved in the delayed onset of therapeutic effects during treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉White, F J -- Wang, R Y -- MH 00378/MH/NIMH NIH HHS/ -- MH-34424/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 9;221(4615):1054-7.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6136093" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antipsychotic Agents/*pharmacology ; Dopamine/*metabolism ; Male ; Metoclopramide/pharmacology ; Mice ; Neurons/metabolism ; Pons/*metabolism ; Rats ; Rats, Inbred Strains ; Substantia Nigra/*metabolism ; Time Factors
    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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