Abstract:
: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.
journal_name
Neurosci Lettjournal_title
Neuroscience lettersauthors
Davis MI,Szarowski D,Turner JN,Morrisett RA,Shain Wdoi
10.1016/s0304-3940(99)00572-8keywords:
subject
Has Abstractpub_date
1999-09-10 00:00:00pages
95-8issue
2eissn
0304-3940issn
1872-7972pii
S0304-3940(99)00572-8journal_volume
272pub_type
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