Differential effects of prenatal and postnatal ACTH or nicotine exposure on 5-HT high affinity uptake in the neonatal rat brain
dc.contributor.author | King, Jean A. | |
dc.contributor.author | Davila-Garcia, Martha | |
dc.contributor.author | Azmitia, Efrain C. | |
dc.contributor.author | Strand, Fleur L. | |
dc.date | 2022-08-11T08:10:27.000 | |
dc.date.accessioned | 2022-08-23T17:09:23Z | |
dc.date.available | 2022-08-23T17:09:23Z | |
dc.date.issued | 1991-01-01 | |
dc.date.submitted | 2010-11-01 | |
dc.identifier.citation | Int J Dev Neurosci. 1991;9(3):281-6. | |
dc.identifier.issn | 0736-5748 (Linking) | |
dc.identifier.pmid | 1656708 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/45806 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.url | http://dx.doi.org/10.1016/0736-5748(91)90048-Q | |
dc.subject | Adrenocorticotropic Hormone | |
dc.subject | Animals | |
dc.subject | Animals, Newborn | |
dc.subject | Aspirin | |
dc.subject | Brain | |
dc.subject | Brain Stem | |
dc.subject | Female | |
dc.subject | Nicotine | |
dc.subject | Pregnancy | |
dc.subject | Prenatal Exposure Delayed Effects | |
dc.subject | Rats | |
dc.subject | Rats, Inbred Strains | |
dc.subject | Serotonin | |
dc.subject | Psychiatry | |
dc.title | Differential effects of prenatal and postnatal ACTH or nicotine exposure on 5-HT high affinity uptake in the neonatal rat brain | |
dc.type | Journal Article | |
dc.source.journaltitle | International journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience | |
dc.source.volume | 9 | |
dc.source.issue | 3 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/psych_pp/336 | |
dc.identifier.contextkey | 1625914 | |
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.submissionpath | psych_pp/336 | |
dc.contributor.department | Department of Psychiatry | |
dc.source.pages | 281-6 |