In vivo activation and in situ BDNF-stimulated nuclear translocation of mitogen-activated/extracellular signal-regulated protein kinase is inhibited by ethanol in the developing rat hippocampus

被引：35

作者：

Davis, MI

Szarowski, D

Turner, JN

Morrisett, RA

Shain, W

机构：

[1] SUNY Albany, Sch Publ Hlth, Dept Biomed Sci, Albany, OR USA

[2] Wadsworth Ctr, Albany, NY USA

[3] Univ Texas, Dept Pharmacol & Toxicol, Coll Pharm, Austin, TX 78712 USA

来源：

NEUROSCIENCE LETTERS | 1999年 / 272卷 / 02期

关键词：

ethanol; brain-derived neurotrophic factor; extracellular signal-regulated kinase; mitogen-activated protein kinase; protein kinase; fetal alcohol syndrome;

D O I：

10.1016/S0304-3940(99)00572-8

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

In order to test the hypothesis that ethanol (EtOH)-induced changes in growth factor signal transduction contribute to the teratogenic effects of EtOH in the developing brain, neonatal rat pups were administered a single dose of EtOH during the brain growth spurt (5 days of age, PN5). Hippocampal mitogen-activated/extracellular signal-regulated protein kinase (MAPK/ERK) activation was analyzed one to 6 h after exposure by electrophoretic-mobility shift assay combined with western blot. Brain-Derived Neurotrophic Factor (BDNF) was used to stimulate ERK in hippocampal slices prepared from PN5 pups and activation and cellular localization was determined with immunofluorescence combined with confocal microscopy. EtOH decreased ERK activation in vivo and decreased nuclear translocation of BDNF-stimulated ERK in situ. These data suggest EtOH-induced inhibition of growth factor signaling may contribute to the development of fetal alcohol syndrome and alcohol-related birth defects. (C) 1999 Elsevier Science Ireland Ltd. All rights reserved.

引用

页码：95 / 98

页数：4

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[1] AN UPDATE ON INCIDENCE OF FAS - FAS IS NOT AN EQUAL-OPPORTUNITY BIRTH-DEFECT [J].