A review of the effects of prenatal or early postnatal ethanol exposure onbrain ligand-gated ion channels

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.