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Ethanol-induced death of postnatal hippocampal neurons.

Abstract：

:Fetal alcohol exposure causes severe neuropsychiatric problems, but mechanisms of the ethanol-associated changes in central nervous system development are unclear. In vivo, ethanol's interaction with N-methyl-D-aspartate (NMDA) and gamma-aminobutyric acid type A (GABA(A)) receptors may cause increased apoptosis in the immature forebrain. We examined whether ethanol affects survival of neonatal hippocampal neurons in primary cultures. A 6-day ethanol exposure killed hippocampal neurons with an LD50 of approximately 25 mM. Elevated extracellular potassium or insulin-related growth factor 1 inhibited cell loss. Although potentiation of GABA(A) receptors or complete block of NMDA receptors also kills hippocampal neurons, pharmacological studies suggest that ethanol's interaction with GABA(A) and NMDA receptors is not sufficient to explain ethanol's effects on neuronal survival. Ca(2+) influx in response to depolarization was depressed >50% by chronic ethanol treatment. We suggest that chronic ethanol may promote neuronal loss through a mechanism affecting Ca(2+) influx in addition to effects on postsynaptic GABA and glutamate receptors.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Moulder KL,Fu T,Melbostad H,Cormier RJ,Isenberg KE,Zorumski CF,Mennerick S

doi

10.1006/nbdi.2002.0523

keywords:

subject

Has Abstract

pub_date

2002-08-01 00:00:00

pages

396-409

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969996102905231

journal_volume

10

pub_type

杂志文章

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