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Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus

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dc.contributor.authorElibol-Can, BİRSEN
dc.contributor.authorKilic, Ertugrul
dc.contributor.authorYuruker, Sinan
dc.contributor.authorJakubowska-Dogru, Ewa
dc.contributor.institutionauthorELİBOL, BİRSEN
dc.date.accessioned2019-10-05T12:58:14Z
dc.date.available2019-10-05T12:58:14Z
dc.date.issued2014-04-01
dc.description.abstractEthanol is known as a potent teratogen responsible for the fetal alcohol syndrome characterized by cognitive deficits especially pronounced in juveniles but ameliorating in adults. Since the mechanisms of these deficits and following partial recovery are not fully elucidated, the aim of the present study was to investigate the process of synaptogenesis in the hippocampus over the first two months of life in control and fetal-alcohol rats. Ethanol was delivered to the pregnant dams by intragastric intubation throughout 7-21 gestation days at the daily dose of 6 g/kg generating a mean blood alcohol level of 246.6 +/- 40.9 mg/dl on gestation day 20. The spine densities as well as the expression of pre- and postsynaptic proteins, synaptophysin (SYP) and PSD-95 protein, were evaluated for three distinct hippocampal regions: CA1, CA2+3, and DG and four postnatal days: PD1, PD10, PD30 and PD60, independently. Our results confirmed an intensive synaptogenesis within the brain spurt period (first 10 postnatal days), however, the temporal pattern of changes in the SYP and PSD-95 expression was different. The ethanol exposure during half of the 1st and the whole 2nd human trimester equivalent resulted in an overall trend toward lower values of synaptic indices at PD1 with a fast recovery from these deficits observed already at PD10. At PD30, around the age when the most pronounced behavioral deficits have been previously reported in juvenile fetal-alcohol subjects, no significant changes were found in either the hippocampal levels of synaptic proteins or in the spine density in principal hippocampal neurons. (C) 2013 ISDN. Published by Elsevier Ltd. All rights reserved.
dc.description.sponsorshipTürkiye Bilimsel Ve Teknolojik Araştırma Kurumu ( Tübitak )
dc.identifier
dc.identifier.citationElibol-Can B., Kilic E., Yuruker S., Jakubowska-Dogru E., -Investigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus-, INTERNATIONAL JOURNAL OF DEVELOPMENTAL NEUROSCIENCE, cilt.33, ss.106-114, 2014
dc.identifier.doi10.1016/j.ijdevneu.2013.12.003
dc.identifier.pubmed24365761
dc.identifier.scopus84892543783
dc.identifier.trdizintrdizin
dc.identifier.urihttps://hdl.handle.net/20.500.12645/1069
dc.identifier.wosWOS:000333002800014
dc.language.isoen
dc.titleInvestigation into the effects of prenatal alcohol exposure on postnatal spine development and expression of synaptophysin and PSD95 in rat hippocampus
dc.typeArticle
dspace.entity.typePublication
local.article.journalnameRHINOLOGY
local.avesis.id18fad9fb-1318-423b-8f67-1d81d6ab5a52
local.avesis.response939
local.publication.isinternational1
relation.isAuthorOfPublication1b1887fb-6b32-44b1-9d9f-416616dc6734
relation.isAuthorOfPublication.latestForDiscovery1b1887fb-6b32-44b1-9d9f-416616dc6734
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