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Effects of postnatal ethanol exposure on neurotrophic factors and signal transduction pathways in rat brain
Author(s) -
Fattori Vittorio,
Abe Shinichi,
Kobayashi Kumiko,
Costa Lucio G.,
Tsuji Ryozo
Publication year - 2008
Publication title -
journal of applied toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.784
H-Index - 87
eISSN - 1099-1263
pISSN - 0260-437X
DOI - 10.1002/jat.1288
Subject(s) - neurotoxicity , neurotrophic factors , signal transduction , mapk/erk pathway , creb , brain derived neurotrophic factor , endocrinology , neurotrophin , medicine , protein kinase b , nerve growth factor , chemistry , toxicity , neuroscience , biology , microbiology and biotechnology , receptor , biochemistry , transcription factor , gene
Exposure to ethanol during development induces severe brain damage, resulting in a number of CNS dysfunctions including microencephaly and mental retardation. Potential targets of ethanol‐induced neurotoxicity include neurotrophic factors and their signal transduction pathways. In the present study, rat pups were given ethanol at the dose of 5 g kg −1 via gavage from postnatal day (PND) 5 to 8, and mRNA expression of nerve growth‐factor (NGF), brain‐derived neurotrophic factor (BDNF), and neurotrophic factor‐3 (NT‐3) in the cerebral cortex was examined, with attention to signal transduction, on PND 8. The mRNA level of BDNF was decreased by ethanol while those of NGF or NT‐3 were not changed. Brain weights were decreased and the levels of phospho‐MAPK, phospho‐p70S6K and phospho Akt were decreased while phosphor‐PKC ζ and phospho‐CREB remained unchanged. These results suggest that BDNF and its related signal pathways involving Akt, MAPK and p70S6K are potential targets of ethanol‐induced developmental neurotoxicity. Copyright © 2007 John Wiley & Sons, Ltd.