ALBERT

All Library Books, journals and Electronic Records Telegrafenberg

feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 1
    Publication Date: 1982-05-07
    Description: Intracerebroventricular administration of oxytocin to virgin female rats that had been ovariectomized and primed with estrogen 48 hours previously induced a rapid onset of full maternal behavior. The maternal behavior persisted and its incidence was dose-related. Tocinoic acid, the ring structure of oxytocin, also rapidly induced the onset of persistent, full maternal behavior. Arginine vasopressin induced persistent maternal behavior, but this behavior had a later onset. Prostaglandin F2 alpha induced strong partial maternal behavior, which showed early onset but did not persist. Many other peptides, ovarian steroids, and prostaglandin E2 were no more effective than saline. These findings suggest that the release of oxytocin and prostaglandin F2 alpha during labor may promote maternal behavior in rats.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Pedersen, C A -- Ascher, J A -- Monroe, Y L -- Prange, A J Jr -- MH-22536/MH/NIMH NIH HHS/ -- MH-32316/MH/NIMH NIH HHS/ -- MH-34933/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1982 May 7;216(4546):648-50.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/7071605" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arginine Vasopressin/pharmacology ; Brain/physiology ; Female ; Injections, Intraventricular ; *Maternal Behavior ; Oxytocin/administration & dosage/*pharmacology ; Rats ; Structure-Activity Relationship
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
  • 2
    Publication Date: 1983-09-02
    Description: To ascertain whether Huntington's chorea and schizophrenia are associated with specific regional alterations in neurotensin, somatostatin, and thyrotropin-releasing hormone, the concentrations of these putative neurotransmitters were measured by radioimmunoassay in postmortem brain samples from patients with Huntington's chorea or schizophrenia. Compared to 50 patients without psychiatric or neurological disease, the patients with Huntington's chorea showed significantly elevated concentrations of all three neuropeptides in the nucleus caudatus. In the nucleus accumbens somatostatin levels were increased threefold, while in the amygdala thyrotropin-releasing hormone levels were elevated. In contrast, the schizophrenics exhibited reduced levels of thyrotropin-releasing hormone in two frontal cortical regions, reduced somatostatin levels in one frontal cortical area, and increased neurotensin levels in one frontal cortical area. None of the differences between the diseased brains and the controls could be accounted for by differences in age, sex, or time between death and autopsy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nemeroff, C B -- Youngblood, W W -- Manberg, P J -- Prange, A J Jr -- Kizer, J S -- MH-32316/MH/NIMH NIH HHS/ -- MH-33127/MH/NIMH NIH HHS/ -- MH-34121/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 1983 Sep 2;221(4614):972-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6136092" target="_blank"〉PubMed〈/a〉
    Keywords: Brain/*metabolism ; Brain Mapping ; Female ; Humans ; Huntington Disease/*metabolism ; Male ; Neurotensin/metabolism ; Neurotransmitter Agents/*metabolism ; Schizophrenia/*metabolism ; Somatostatin/metabolism ; Thyrotropin-Releasing Hormone/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Location Call Number Expected Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...