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Prenatal ethanol exposure enhances NMDAR‐dependent long‐term potentiation in the adolescent female dentate gyrus
Author(s) -
Titterness Andrea K.,
Christie Brian R.
Publication year - 2012
Publication title -
hippocampus
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.767
H-Index - 155
eISSN - 1098-1063
pISSN - 1050-9631
DOI - 10.1002/hipo.20849
Subject(s) - long term potentiation , dentate gyrus , hippocampus , synaptic plasticity , prenatal stress , in utero , corticosterone , neuroscience , ethanol , endocrinology , medicine , psychology , chemistry , gestation , fetus , pregnancy , biology , biochemistry , hormone , receptor , genetics
The dentate gyrus (DG) is a region of the hippocampus intimately involved with learning and memory. Prenatal exposure to either stress or ethanol can reduce long‐term potentiation (LTP) in the male hippocampus but there is little information on how these prenatal events affect LTP in the adolescent female hippocampus. Previous studies suggest that deleterious effects of PNEE can, in part, be mediated by corticosterone, suggesting that prenatal stress might further enhance any alterations to LTP induced PNEE. When animals were exposed to a combination of prenatal stress and PNEE distinct sex differences emerged. Exposure to ethanol throughout gestation significantly reduced DG LTP in adolescent males but enhanced LTP in adolescent females. Combined exposure to stress and ethanol in utero reduced the ethanol‐induced enhancement of LTP in females. On the other hand, exposure to stress and ethanol in utero did not alter the ethanol‐induced reduction of LTP in males. These results indicate that prenatal ethanol and prenatal stress produce sex‐specific alterations in synaptic plasticity in the adolescent hippocampus. © 2010 Wiley Periodicals, Inc., Inc.