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Prenatal ethanol intoxication and maternal intubation stress alter cell survival and apoptosis in the postnatal development of rat hippocampus.

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dc.contributor.authorSahbaz, CD
dc.contributor.authorElibol, BİRSEN
dc.contributor.authorBeker, M
dc.contributor.authorKilic, U
dc.contributor.authorJakubowska-Doğru, E
dc.contributor.institutionauthorELİBOL, BİRSEN
dc.contributor.institutionauthorŞAHBAZ, ÇIĞDEM DILEK
dc.date.accessioned2019-10-05T13:11:14Z
dc.date.available2019-10-05T13:11:14Z
dc.date.issued2019-01-01
dc.description.abstractIt is well known that the fetal ethanol exposure and prenatal stress may have adverse effects on brain development. Interestingly, some morphological and functional recovery from their teratogenic effects that take place during brain maturation. However, mechanisms that underlie this recovery are not fully elucidated. The aim of this study was to examine whether the postnatal attenuation of fetal alcohol - and maternal stress‑induced morphological and functional deficits correlates with compensatory changes in the expression/activation of the brain proteins involved in inflammation, cell survival and apoptosis. In this project, we investigated the hippocampus which belongs to the brain regions most susceptible to the adverse effects of prenatal ethanol exposure. Pregnant rat dams were administered ethanol (A) or isocaloric glucose solution (IC) by a gastric intubation during gestational days 7-20. The pure control group received ad libitum laboratory chow and water with no other treatment. The hippocampi of fetal-ethanol and control pups were examined at the postnatal day (PD)1, PD10, PD30 and PD60. Moderate fetal-ethanol exposure and prenatal intubation stress caused a significant increase in molecular factors relating to inflammation (iNOS) and cell survival/apoptosis pathways (PTEN, GSK-3 and ERK) at birth, with a rapid compensation from these developmental deficits upon removal of alcohol at PD10. Indeed, an increase in ERK1/2 and JNK1/2 activation at PD30 was observed with ethanol consumption. It indicates that the recovery process in A and IC brains started soon after the birth upon the ethanol and stressor withdrawal and continued until the adulthood.en
dc.description.sponsorshipBezmialem Vakıf Üniversitesi
dc.description.sponsorshipTürkiye Bilimsel Ve Teknolojik Araştırma Kurumu ( Tubitak )
dc.identifier10.14235/bs.2014.155
dc.identifier.citationElibol B., Beker M., Sahbaz C., Kilic U., Jakubowska-Doğru E., -Prenatal ethanol intoxication and maternal intubation stress alter cell survival and apoptosis in the postnatal development of rat hippocampus.-, Acta neurobiologiae experimentalis, cilt.79, ss.133-147, 2019
dc.identifier.doi10.21307/ane-2019-012
dc.identifier.pubmed31342950
dc.identifier.scopus85070512296
dc.identifier.urihttps://hdl.handle.net/20.500.12645/1540
dc.identifier.wosWOS:000476617700003
dc.language.isoen
dc.rightsinfo:eu-repo/semantics/openAccessen
dc.titlePrenatal ethanol intoxication and maternal intubation stress alter cell survival and apoptosis in the postnatal development of rat hippocampus.
dc.typeArticle
dspace.entity.typePublication
local.article.journalnameBezmialem Science
local.avesis.id24b50931-7b7a-4ba7-8c23-e8c93ea2dff7
local.avesis.response1410
local.publication.isinternational1
relation.isAuthorOfPublication1b1887fb-6b32-44b1-9d9f-416616dc6734
relation.isAuthorOfPublication5c311165-fcb8-4dfa-acec-7b954de29bfc
relation.isAuthorOfPublication.latestForDiscovery5c311165-fcb8-4dfa-acec-7b954de29bfc
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