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Neg , a nerve growth factor–stimulated gene expressed by fetal neocortical neurons that is downregulated by ethanol
Author(s) -
Miller Michael W.,
Jacobs Julie S.,
Yokoyama Ruth
Publication year - 2003
Publication title -
journal of comparative neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.855
H-Index - 209
eISSN - 1096-9861
pISSN - 0021-9967
DOI - 10.1002/cne.10651
Subject(s) - nerve growth factor , biology , neuroprotection , neurotrophin , gene expression , downregulation and upregulation , microbiology and biotechnology , neurotrophin 3 , programmed cell death , in situ hybridization , endocrinology , medicine , gene , brain derived neurotrophic factor , neurotrophic factors , neuroscience , biochemistry , apoptosis , receptor
Neurotrophins are critical for neuronal development, plasticity, and survival. Ethanol affects these processes. We tested the hypothesis that ethanol inhibits nerve growth factor (NGF)–stimulated gene expression. Dissociated cultures of fetal cortical neurons were treated with NGF and/or ethanol. NGF sustained cell viability and reduced the incidence of terminal uridylated nick‐end labeling and pyknosis. Ethanol eliminated these effects and induced neuronal death. Differential display of mRNA showed that one gene fragment (245 bp) was expressed by cells treated with NGF alone; ethanol blocked its expression. This fragment, named neg (nerve growth factor–stimulated, ethanol‐depressed gene), has high nucleotide identity with genes from human myeloid cells and murine lymphocytes. Ribonuclease protection assay and in situ hybridization verified NGF upregulation and ethanol antagonism. Thus, ethanol specifically alters the expression of a gene that appears to be involved in NGF‐mediated neuroprotection. J. Comp. Neurol. 460:212–222, 2003. © 2003 Wiley‐Liss, Inc.