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  • Articles  (45)
  • Rats, Inbred Strains
  • 1985-1989  (12)
  • 1980-1984  (33)
  • 1925-1929
  • 1987  (12)
  • 1983  (33)
  • Physics  (45)
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  • Articles  (45)
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  • 1985-1989  (12)
  • 1980-1984  (33)
  • 1925-1929
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  • 1
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-03-25
    Description: The activity of 7,12-dimethylbenz[a]anthracene hydroxylase in the rat ovary is several times higher in the proestrous phase of the estrous cycle than in the estrous and metestrous plus diestrous phases. Administration of gonadotropin leads to a similar increase in the capacity of the ovary to metabolize xenobiotics. This variation in the activity of 7,12-dimethylbenz[a]anthracene hydroxylase during the estrous cycle may be related to the marked changes in the incidence of ovarian cancer during menopause and in women taking contraceptive pills.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bengtsson, M -- Rydstrom, J -- New York, N.Y. -- Science. 1983 Mar 25;219(4591):1437-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6681915" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aryl Hydrocarbon Hydroxylases/*metabolism ; Cytochrome P-450 Enzyme System/metabolism ; Epoxide Hydrolases/metabolism ; *Estrus ; Female ; Glutathione Transferase/metabolism ; Gonadotropins, Equine/*pharmacology ; Metestrus ; Ovary/*physiology ; Pregnancy ; Proestrus ; Quinone Reductases/metabolism ; Rats ; Rats, Inbred Strains
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  • 2
    Publication Date: 1983-06-17
    Description: Animals with a history of receiving daily injections of +-amphetamine in a specific environment showed a placebo effect (enhanced activity) when injected with saline and placed there; control animals with similar but dissociated drug histories and experience with the test chamber failed to show the effect. The dopamine receptor blocker pimozide antagonized the establishment of conditioning. However, the same dose of pimozide, when given to previously conditioned animals on the placebo test day, failed to antagonize the expression of conditioned activity. Thus, during conditioning dopaminergic neurons mediated a change that subsequently influenced behavior even when dopaminergic systems were blocked. Although schizophrenia may be related to hyperfunctioning of dopamine, neuroleptic drugs, which block dopamine receptors on their first administration, do not have therapeutic effects for a number of days. The results of the pimozide experiments may resolve this paradox.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Beninger, R J -- Hahn, B L -- New York, N.Y. -- Science. 1983 Jun 17;220(4603):1304-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857251" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Conditioning (Psychology)/*drug effects/physiology ; Dextroamphetamine/antagonists & inhibitors/*pharmacology ; Humans ; Male ; Pimozide/*pharmacology ; Rats ; Rats, Inbred Strains ; Receptors, Dopamine/physiology ; Reinforcement (Psychology) ; Schizophrenia/physiopathology
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  • 3
    Publication Date: 1983-07-08
    Description: Microvoltammetric electrodes were used to monitor dopamine released in the caudate nucleus of the rat after electrical stimulation of the medial forebrain bundle. The time resolution of the technique is sufficient to determine in vivo concentration changes on a time scale of seconds. Direct evidence identifying the substance released as dopamine was obtained both voltammetrically and pharmacologically. Administration of alpha-methyl-p-tyrosine terminates the release of dopamine, although tissue stores of dopamine are still present. Thus there appears to be a compartment for dopamine storage that is not available for immediate release. This compartment appears to be mobilized by amfonelic acid, since administration of this agent after alpha-methyl-p-tyrosine returns the concentration of dopamine released by electrical stimulation to 75 percent of the original amount.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ewing, A G -- Bigelow, J C -- Wightman, R M -- KO 4 NS000356/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Jul 8;221(4606):169-71.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6857277" target="_blank"〉PubMed〈/a〉
    Keywords: Amphetamine/pharmacology ; Animals ; Caudate Nucleus/drug effects/*metabolism ; Dopamine/*metabolism ; Male ; Methyltyrosines/pharmacology ; Microelectrodes ; Naphthyridines/pharmacology ; Rats ; Rats, Inbred Strains ; alpha-Methyltyrosine
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  • 4
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1983-08-12
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Fox, J L -- New York, N.Y. -- Science. 1983 Aug 12;221(4611):625-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6603019" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Animals, Laboratory ; Jurisprudence ; Mice ; *Mice, Inbred BALB C ; Rats ; Rats, Inbred Lew ; Rats, Inbred Strains ; Research ; United States ; Wisconsin
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  • 5
    Publication Date: 1983-05-27
    Description: Adenosine receptors were made visible on light microscopy by autoradiography with tritiated cyclohexyladenosine. In the cerebellum, adenosine receptors were absent in Weaver mice, which lack granule cells, and were displaced in Reeler mice, which have displacements of granule cells. Thus, adenosine receptors appear to be located on the axon terminals of excitatory granule cells in the cerebellum. Removal of one eye of a rat depleted adenosine receptors in the contralateral superior colliculus, suggesting that the receptors occur on axon terminals of excitatory projections from retinal ganglion cells. The presence of adenosine receptors on excitatory axon terminals may explain synaptic inhibition by adenosine and the behavioral effects of xanthines.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goodman, R R -- Kuhar, M J -- Hester, L -- Snyder, S H -- DA-00266/DA/NIDA NIH HHS/ -- MH-18501/MH/NIMH NIH HHS/ -- NS-16375/NS/NINDS NIH HHS/ -- etc. -- New York, N.Y. -- Science. 1983 May 27;220(4600):967-9.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6302841" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine/*physiology ; Animals ; Autoradiography ; Axons/*physiology ; Cerebellum/physiology ; Corpus Striatum/physiology ; Hippocampus/physiology ; Mice ; Mice, Neurologic Mutants ; Rats ; Rats, Inbred Strains ; Receptors, Cell Surface/*physiology ; Receptors, Purinergic ; Retinal Ganglion Cells/physiology ; Synaptic Membranes/physiology ; Thalamus/physiology
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  • 6
    Publication Date: 1983-04-29
    Description: Long-term treatment of rats with atropine induced large increases in the numbers of muscarinic receptors and receptors for vasoactive intestinal polypeptide in the salivary glands. Since receptors for vasoactive intestinal polypeptide coexist with muscarinic receptors on the same neurons in this preparation, the results suggest that a drug that alters the sensitivity of one receptor may also affect the sensitivity of the receptor for a costored transmitter and in this way contribute to the therapeutic or side effects of the drugs.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hedlund, B -- Abens, J -- Bartfai, T -- New York, N.Y. -- Science. 1983 Apr 29;220(4596):519-21.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6132446" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/*pharmacology ; Gastrointestinal Hormones/*metabolism ; Male ; Neurotransmitter Agents/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Cholinergic/*drug effects ; Receptors, Muscarinic/analysis/*drug effects ; Salivary Glands/analysis/innervation ; Vasoactive Intestinal Peptide/analysis/*metabolism
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  • 7
    Publication Date: 1983-04-15
    Description: Administration of pilocarpine or physostigmine to rats treated with lithium chloride produced sustained limbic seizures, widespread brain damage, and increased concentrations of D-myo-inositol-1-phosphate (a metabolite of the phosphoinositides, lipids involved in membrane receptor function) in the brain. The syndrome was preventable with atropine. The physostigmine doses and concentrations of blood lithium that caused the syndrome are similar to those considered appropriate for psychiatric chemotherapy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Honchar, M P -- Olney, J W -- Sherman, W R -- MH-14677/MH/NIMH NIH HHS/ -- MH-38894/MH/NIMH NIH HHS/ -- NS-05159/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1983 Apr 15;220(4594):323-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6301005" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Atropine/pharmacology ; Brain Chemistry/drug effects ; Chlorides/adverse effects ; Drug Interactions ; Humans ; Inositol/analogs & derivatives/analysis ; *Inositol Phosphates ; Lithium/*adverse effects ; Lithium Chloride ; Male ; Parasympathomimetics/*adverse effects ; Physostigmine/adverse effects ; Pilocarpine/adverse effects ; Rats ; Rats, Inbred Strains ; Seizures/*chemically induced ; Substance-Related Disorders/*etiology
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  • 8
    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
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  • 9
    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
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  • 10
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    American Association for the Advancement of Science (AAAS)
    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
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  • 11
    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
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  • 12
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    American Association for the Advancement of Science (AAAS)
    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
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  • 13
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    American Association for the Advancement of Science (AAAS)
    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
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  • 14
    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
    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
    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
    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
    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
    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
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
    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
    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
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
    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
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    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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    Unknown
    American Association for the Advancement of Science (AAAS)
    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
    Publication Date: 1987-11-13
    Description: The long-term effects of excitotoxic lesions in the nucleus basalis magnocellularis of the rat were found to mimic several neuropathological and chemical changes associated with Alzheimer's disease. Neuritic plaque-like structures, neurofibrillary changes, and neuronal atrophy or loss were observed in the frontoparietal cortex, hippocampus, amygdala, and entorhinal cortex 14 months after the lesions were made. Cholinergic markers in neocortex were reduced, while catecholamine and indoleamine metabolism was largely unaffected at this time. Bilateral lesions of the nucleus basalis magnocellularis increased somatostatin and neuropeptide Y in the cortex of the rat by at least 138 and 284 percent, respectively, suggesting a functional interaction between cholinergic and peptidergic neurons that may differ from that in Alzheimer's disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arendash, G W -- Millard, W J -- Dunn, A J -- Meyer, E M -- HD 17933/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Nov 13;238(4829):952-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biology, University of South Florida, Tampa 33620.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2890210" target="_blank"〉PubMed〈/a〉
    Keywords: Acetylcholinesterase/metabolism ; Animals ; Biogenic Amines/metabolism ; Brain/metabolism/*pathology ; Cerebral Cortex/metabolism/*pathology ; Choline/metabolism ; Choline O-Acetyltransferase/metabolism ; Male ; Neuropeptide Y/analysis ; Olivary Nucleus/*physiology ; Organ Specificity ; Rats ; Rats, Inbred Strains ; Somatostatin/analysis
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  • 31
    Publication Date: 1987-10-23
    Description: Intraperitoneal administration of human recombinant interleukin-1 (IL-1) to rats can increase blood levels of corticosterone and adrenocorticotropic hormone (ACTH). The route by which IL-1 affects pituitary-adrenal activity is unknown. That the IL-1-induced pituitary-adrenal activation involves an increased secretion of corticotropin-releasing factor (CRF) is indicated by three lines of evidence. First, immunoneutralization of CRF markedly attenuated the IL-1-induced increase of ACTH blood levels. Second, after blockade of fast axonal transport in hypothalamic neurons by colchicine, IL-1 administration decreased the CRF immunostaining in the median eminence, indicating an enhanced release of CRF in response to IL-1. Third, IL-1 did not stimulate ACTH release from primary cultures of anterior pituitary cells. These data further support the notion of the existence of an immunoregulatory feedback circuit between the immune system and the brain.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Berkenbosch, F -- van Oers, J -- del Rey, A -- Tilders, F -- Besedovsky, H -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):524-6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pharmacology, Medical Faculty, Free University, Amsterdam, the Netherlands.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2443979" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Glands/physiology ; Adrenocorticotropic Hormone/secretion ; Animals ; Axonal Transport/drug effects ; Colchicine/pharmacology ; Corticotropin-Releasing Hormone/immunology/*physiology ; Fluorescent Antibody Technique ; Hypothalamus/*metabolism ; Immune Sera/pharmacology ; Interleukin-1/*physiology ; Male ; Median Eminence/metabolism ; Neurons/*metabolism ; Pituitary Gland, Anterior/physiology ; Rats ; Rats, Inbred Strains
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  • 32
    Publication Date: 1987-10-23
    Description: Exposure to bacterial endotoxins has long been known to stimulate the release of anterior pituitary hormones; administration of endotoxin was at one time a common clinical test of anterior pituitary function. Endotoxin is a potent stimulus for production of the endogenous pyrogenic protein, interleukin-1 (IL-1), by macrophages and monocytes. The possibility that IL-1 has a direct effect on the secretion of hormones by rat pituitary cells in a monolayer culture was investigated. Recombinant human IL-1 beta stimulated the secretion of adrenocorticotropic hormone, luteinizing hormone, growth hormone, and thyroid-stimulating hormone. Increased hormone secretion into culture supernatants was found with IL-1 concentrations ranging from 10(-9) M to 10(-12) M. Prolactin secretion by the monolayers was inhibited by similar doses. These concentrations of IL-1 are within the range reported for IL-1 in serum, suggesting that IL-1 generated peripherally by mononuclear immune cells may act directly on anterior pituitary cells to modulate hormone secretion in vivo. Incubation of IL-1 solutions with antibody to IL-1 neutralized these actions. These pituitary effects of IL-1 suggest that this monokine may be an important regulator of the metabolic adaptations to infectious stressors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bernton, E W -- Beach, J E -- Holaday, J W -- Smallridge, R C -- Fein, H G -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):519-21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Neuropsychiatry, Walter Reed Army Institute of Research, Washington, D.C. 20307-5100.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821620" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenocorticotropic Hormone/secretion ; Animals ; Cells, Cultured ; Dinoprostone ; Female ; Growth Hormone/secretion ; Humans ; Infection/physiopathology ; Inflammation/physiopathology ; Interleukin-1/*physiology ; Luteinizing Hormone/secretion ; Pituitary Gland, Anterior/*secretion ; Pituitary Hormones, Anterior/*secretion ; Prolactin/secretion ; Prostaglandins E/secretion ; Rats ; Rats, Inbred Strains ; Recombinant Proteins/pharmacology ; Thyrotropin/secretion
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  • 33
    Publication Date: 1987-09-11
    Description: The role of polypeptide growth factors in the processes of inflammation and repair was investigated by analyzing the influence of transforming growth factor-beta (TGF-beta), applied directly to linear incisions made through rat dorsal skin. A dose-dependent, direct stimulatory effect of a single application of TGF-beta on the breaking strength of healing incisional wounds was demonstrated. An increase in maximum wound strength of 220 percent of control was observed at 5 days; the healing rate was accelerated by approximately 3 days for at least 14 days after production of the wound and application of TGF-beta. These increases in wound strength were accompanied by an increased influx of mononuclear cells and fibroblasts and by marked increases in collagen deposition at the site of application of TGF-beta. TGF-beta is thus a potent pharmacologic agent that can accelerate wound healing in rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Mustoe, T A -- Pierce, G F -- Thomason, A -- Gramates, P -- Sporn, M B -- Deuel, T F -- New York, N.Y. -- Science. 1987 Sep 11;237(4820):1333-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2442813" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Growth Substances/*pharmacology ; Male ; Peptides/*pharmacology ; Rats ; Rats, Inbred Strains ; Staining and Labeling ; Transforming Growth Factors ; Wound Healing/*drug effects ; Wounds, Penetrating/*pathology
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  • 34
    Publication Date: 1987-09-04
    Description: Although cocaine binds to several sites in the brain, the biochemical receptor mechanism or mechanisms associated with its dependence producing properties are unknown. It is shown here that the potencies of cocaine-like drugs in self-administration studies correlate with their potencies in inhibiting [3H]mazindol binding to the dopamine transporters in the rat striatum, but not with their potencies in binding to a large number of other presynaptic and postsynaptic binding sites. Thus, the cocaine receptor related to substance abuse is proposed to be the one associated with dopamine uptake inhibition.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ritz, M C -- Lamb, R J -- Goldberg, S R -- Kuhar, M J -- New York, N.Y. -- Science. 1987 Sep 4;237(4819):1219-23.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2820058" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/drug effects/*metabolism ; Cattle ; Cocaine/administration & dosage/*pharmacology ; Corpus Striatum/metabolism ; Dopamine/metabolism ; Haplorhini ; Male ; Mazindol/metabolism ; Norepinephrine/metabolism ; Rats ; Rats, Inbred Strains ; Receptors, Adrenergic/drug effects/metabolism ; Receptors, Dopamine/drug effects/*metabolism ; Receptors, Serotonin/drug effects/metabolism ; Self Administration ; Serotonin/metabolism
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  • 35
    Publication Date: 1987-12-11
    Description: One mechanism considered responsible for the hypercalcemia that frequently accompanies malignancy is secretion by the tumor of a circulating factor that alters calcium metabolism. The structure of a tumor-secreted peptide was recently determined and found to be partially homologous to parathyroid hormone (PTH). The amino-terminal 1-34 region of the factor was synthesized and evaluated biologically. In vivo it produced hypercalcemia, acted on bone and kidney, and stimulated 1,25-dihydroxy-vitamin D3 formation. In vitro it interacted with PTH receptors and, in some systems, was more potent than PTH. These studies support a long-standing hypothesis regarding pathogenesis of malignancy-associated hypercalcemia.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Horiuchi, N -- Caulfield, M P -- Fisher, J E -- Goldman, M E -- McKee, R L -- Reagan, J E -- Levy, J J -- Nutt, R F -- Rodan, S B -- Schofield, T L -- AR 36446/AR/NIAMS NIH HHS/ -- AR 39191/AR/NIAMS NIH HHS/ -- New York, N.Y. -- Science. 1987 Dec 11;238(4833):1566-8.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Regional Bone Center, Helen Hayes Hospital (New York State Department of Health), West Haverstraw 10993.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3685994" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Calcium/blood ; Humans ; Hypercalcemia/etiology ; Neoplasms/*physiopathology ; Parathyroid Glands/physiology ; Parathyroid Hormone/pharmacology/*physiology ; Peptides/*physiology ; Rats ; Rats, Inbred Strains ; Thyroidectomy
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  • 36
    Publication Date: 1987-10-23
    Description: There is now evidence that the immune system, during times of infectious challenge, can stimulate the secretion of glucocorticoids, the adrenal steroids that mediate important aspects of the response to stress. Specifically, secretion of interleukin-1 (IL-1), a monocyte lymphokine secreted after infection, appears at least in part responsible for this effect. Glucocorticoids are secreted in response to a neuroendocrine cascade involving, first, the brain, then the pituitary, and finally the adrenal gland. In this report, human IL-1 is shown to activate the adrenocortical axis at the level of the brain, stimulating the release of the controlling hormone corticotropin-releasing factor (CRF) from the hypothalamus. Infusion of IL-1 induced a significant secretion of CRF into the circulation exiting the hypothalamus, whereas immunoneutralization of CRF blocked the stimulatory effect of IL-1 on glucocorticoid secretion. IL-1 appeared to have no acute direct stimulatory effects on the pituitary or adrenal components of this system. Furthermore, IL-1 did not cause a nonspecific release of other hypothalamic hormones. Thus, the lymphokine acts in a specific manner to activate the adrenocortical axis at the level of the brain; this effect appears to be unrelated to the known pyrogenic effects of IL-1 within the hypothalamus.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sapolsky, R -- Rivier, C -- Yamamoto, G -- Plotsky, P -- Vale, W -- AA06420/AA/NIAAA NIH HHS/ -- AM26741/AM/NIADDK NIH HHS/ -- New York, N.Y. -- Science. 1987 Oct 23;238(4826):522-4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Stanford University, CA 94305.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2821621" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex/physiology ; Adrenocorticotropic Hormone/secretion ; Animals ; Cell Line ; Corticosterone/secretion ; Corticotropin-Releasing Hormone/*secretion ; Hypothalamus/*secretion ; Immunologic Techniques ; Interleukin-1/*physiology ; Male ; Pituitary Gland, Anterior/secretion ; Pituitary Neoplasms/secretion ; Rats ; Rats, Inbred Strains
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  • 37
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-01-09
    Description: Cholinergic neuronal degeneration after axotomy has been proposed to be due to the loss of a retrogradely transported neurotrophic factor, possibly nerve growth factor (NGF). To test this hypothesis, NGF was continuously infused into the lateral ventricles of adult rats that had received bilateral lesions of all cholinergic axons projecting from the medial septum to the dorsal hippocampus. After 2 weeks of NGF treatment, identification of cholinergic neurons by the presence of the biosynthetic enzyme choline acetyltransferase revealed a dramatic increase (350%) in the survival of the axotomized septal cholinergic neurons. Thus, NGF or an NGF-like molecule can act as a neurotrophic factor for these neurons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kromer, L F -- AG-06648/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 1987 Jan 9;235(4785):214-6.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3798108" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain Injuries/*drug therapy/pathology ; Cell Survival ; Choline O-Acetyltransferase/metabolism ; Cholinergic Fibers/pathology ; Female ; Hippocampus/injuries ; Nerve Growth Factors/administration & dosage/*therapeutic use ; Neurons/enzymology/*pathology ; Rats ; Rats, Inbred Strains ; Septum Pellucidum/injuries
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  • 38
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-02-27
    Description: Although hypothyroidism (with concomitant increased levels of thyroid-stimulating hormone) has been associated with elevated plasma vasopressin, the role that vasopressin plays in controlling thyroid-stimulating hormone secretion from the adenohypophysis is not understood. In two in vitro pituitary cell systems, vasopressin caused a specific and dose-related release of thyroid-stimulating hormone from cells that was equal in potency to that elicited by thyrotropin-releasing hormone, the primary acknowledged regulator of thyroid-stimulating hormone release. When injected into the hypothalamus, however, vasopressin specifically inhibited the release of thyroid-stimulating hormone. Thus, vasopressin may exert differential regulatory effects on thyroid-stimulating hormone secretion in the hypothalamus and pituitary gland.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lumpkin, M D -- Samson, W K -- McCann, S M -- HD-09988/HD/NICHD NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 27;235(4792):1070-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2881350" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/*pharmacology/physiology ; Hypothalamus/drug effects/secretion ; Male ; Oxytocin/pharmacology ; Perfusion ; Pituitary Gland, Anterior/drug effects/*secretion ; Rats ; Rats, Inbred Strains ; Somatostatin/pharmacology ; Thyrotropin/*secretion ; Thyrotropin-Releasing Hormone/pharmacology
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  • 39
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    Unknown
    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-02-13
    Description: In order to determine whether the blood-brain barrier was present in transplants of central nervous tissue, fetal neocortex, which already possesses blood-brain and blood-cerebrospinal fluid barriers to protein, was grafted into the undamaged fourth ventricle or directly into the neocortex of recipient rats. Horseradish peroxidase or a conjugated human immunoglobulin G-peroxidase molecule was systemically administered into the host. These proteins were detected within the cortical transplants within 2 minutes regardless of the age of the donor or postoperative time. At later times these compounds, which normally do not cross the blood-brain barrier, inundated the grafts and adjacent host brain and also entered the cerebrospinal fluid. Endogenous serum albumin detected immunocytochemically in untreated hosts had a comparable although less extensive distribution. Thus, transplants of fetal central nervous tissue have permanent barrier dysfunction, probably due to microvascular changes, and are not integrated physiologically within the host. Blood-borne compounds, either systemically administered or naturally occurring, which should never contact normal brain tissue, have direct access to these transplants and might affect neuronal function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rosenstein, J M -- NS-17468/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 1987 Feb 13;235(4790):772-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2433767" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axonal Transport ; *Blood-Brain Barrier ; Brain/*physiology ; Cerebral Cortex/physiology/*transplantation ; Cerebral Ventricles/physiology ; Female ; Fetus ; Gestational Age ; Horseradish Peroxidase/*metabolism ; Immunoglobulin G/metabolism ; Peroxidases/*metabolism ; Pregnancy ; Rats ; Rats, Inbred Strains
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  • 40
    Publication Date: 1987-03-06
    Description: Under the influence of estrogen, uterine smooth muscle becomes highly excitable, generating spontaneous and prolonged bursts of action potentials. In a study of the mechanisms by which this transition in excitability occurs, polyadenylated RNA from the uteri of estrogen-treated rats was injected into Xenopus oocytes. The injected oocytes expressed a novel voltage-dependent potassium current. This current was not observed in oocytes injected with RNA from several other excitable tissues, including rat brain and uterine smooth muscle from ovariectomized rats not treated with estrogen. The activation of this current on depolarization was exceptionally slow, particularly for depolarizations from relatively negative membrane potentials. Such a slowly activating channel may play an important role in the slow, repetitive bursts of action potentials in the myometrium.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Boyle, M B -- Azhderian, E M -- MacLusky, N J -- Naftolin, F -- Kaczmarek, L K -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1221-4.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/2434999" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Calcium/pharmacology ; Egtazic Acid/pharmacology ; Female ; Injections ; Ion Channels/*metabolism ; Oocytes/*metabolism ; Potassium/*metabolism ; RNA/*pharmacology ; Rats ; Rats, Inbred Strains ; Time Factors ; Uterus/*metabolism ; Xenopus
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  • 41
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    American Association for the Advancement of Science (AAAS)
    Publication Date: 1987-03-06
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miczek, K A -- Weerts, E M -- New York, N.Y. -- Science. 1987 Mar 6;235(4793):1127-8.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/3823870" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Azides/*adverse effects ; Benzodiazepines/*adverse effects ; Male ; Rats ; Rats, Inbred Strains ; Saimiri ; Seizures/*chemically induced
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  • 42
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    American Association for the Advancement of Science (AAAS)
    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
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  • 43
    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
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  • 44
    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
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  • 45
    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
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