Et. Costa et al., A review of the effects of prenatal or early postnatal ethanol exposure onbrain ligand-gated ion channels, ALC CLIN EX, 24(5), 2000, pp. 706-715
Background: Ligand-gated ion channels mediate fast excitatory and inhibitor
y synaptic transmission in the developing central nervous system. These cha
nnels have been shown to have roles in neuronal proliferation, differentiat
ion, and programmed cell death. Numerous studies over the past 10 years ind
icate that prenatal and/or early postnatal ethanol exposure affects neurotr
ansmitter-gated ion channels.
Methods: We conducted a review of the relevant literature, identified by a
computer-assisted literature search. This review presents an overview of st
udies performed with experimental preparations from the brains of rodents e
xposed to ethanol in utero and/or during the neonatal period and summarizes
some of the salient issues that have developed in the course of these inve
stigations. Differences in ethanol exposure paradigms and blood alcohol con
centrations obtained in these studies are highlighted, and directions for f
uture research are suggested.
Results: Most studies have focused on the effects of prenatal or early post
natal ethanol exposure on NMDA receptors. These studies show that ethanol e
xposure affects ligand binding, subunit expression, and function of this re
ceptor. Fewer studies have examined ethanol's effects on ligand-gated ion c
hannels other than NMDA receptors. For instance, a study reported changes i
n ligand binding to hippocampal kainate receptors. Another study found alte
rations in modulation of GABA(A) receptors by benzodiazepines and neuroster
oids.
Conclusions: These studies suggest that the effects of ethanol on brain ion
channels may have a role in the pathophysiology of Alcohol-Related Neurode
velopmental Disorders and Fetal Alcohol Syndrome.