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dc.contributor.authorKing, Jean A.
dc.contributor.authorDavila-Garcia, Martha
dc.contributor.authorAzmitia, Efrain C.
dc.contributor.authorStrand, Fleur L.
dc.date2022-08-11T08:10:27.000
dc.date.accessioned2022-08-23T17:09:23Z
dc.date.available2022-08-23T17:09:23Z
dc.date.issued1991-01-01
dc.date.submitted2010-11-01
dc.identifier.citationInt J Dev Neurosci. 1991;9(3):281-6.
dc.identifier.issn0736-5748 (Linking)
dc.identifier.pmid1656708
dc.identifier.urihttp://hdl.handle.net/20.500.14038/45806
dc.description.abstractThese studies were designed to examine the differential effects of prenatal or postnatal administration of ACTH 1-39 and nicotine, on 5-HT high affinity uptake in brainstem and hippocampal synaptosomes. ACTH was administered prenatally (to pregnant dams) and postnatally to the neonates. Postnatal administration of ACTH significantly increased high-affinity 5-HT uptake in the hippocampus and especially the brainstem at both 7 and 21 days after birth. Prenatal ACTH, on the other hand, transiently increased 5-HT uptake in only the brainstem at 7 days, a change that was reversed at 21 days. While the effects of postnatal nicotine administration were essentially the same as those of postnatal ACTH treatment, prenatal nicotine, unlike ACTH, did not alter 5-HT uptake in 7-day-old rats but did reduce uptake in both tissues at 21 days. The observation that postnatal nicotine mimics the effects of postnatal ACTH and that nicotine stimulates ACTH release, suggests that the postnatal effects of nicotine may be exerted through ACTH.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=1656708&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1016/0736-5748(91)90048-Q
dc.subjectAdrenocorticotropic Hormone
dc.subjectAnimals
dc.subjectAnimals, Newborn
dc.subjectAspirin
dc.subjectBrain
dc.subjectBrain Stem
dc.subjectFemale
dc.subjectNicotine
dc.subjectPregnancy
dc.subjectPrenatal Exposure Delayed Effects
dc.subjectRats
dc.subjectRats, Inbred Strains
dc.subjectSerotonin
dc.subjectPsychiatry
dc.titleDifferential effects of prenatal and postnatal ACTH or nicotine exposure on 5-HT high affinity uptake in the neonatal rat brain
dc.typeJournal Article
dc.source.journaltitleInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
dc.source.volume9
dc.source.issue3
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/psych_pp/336
dc.identifier.contextkey1625914
html.description.abstract<p>These studies were designed to examine the differential effects of prenatal or postnatal administration of ACTH 1-39 and nicotine, on 5-HT high affinity uptake in brainstem and hippocampal synaptosomes. ACTH was administered prenatally (to pregnant dams) and postnatally to the neonates. Postnatal administration of ACTH significantly increased high-affinity 5-HT uptake in the hippocampus and especially the brainstem at both 7 and 21 days after birth. Prenatal ACTH, on the other hand, transiently increased 5-HT uptake in only the brainstem at 7 days, a change that was reversed at 21 days. While the effects of postnatal nicotine administration were essentially the same as those of postnatal ACTH treatment, prenatal nicotine, unlike ACTH, did not alter 5-HT uptake in 7-day-old rats but did reduce uptake in both tissues at 21 days. The observation that postnatal nicotine mimics the effects of postnatal ACTH and that nicotine stimulates ACTH release, suggests that the postnatal effects of nicotine may be exerted through ACTH.</p>
dc.identifier.submissionpathpsych_pp/336
dc.contributor.departmentDepartment of Psychiatry
dc.source.pages281-6


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