Background: Ligand-gated ion channels mediate fast excitatory and inhibitory synaptic transmission in the developing central nervous system. These channels have been shown to have roles in neuronal proliferation, differentiation, and programmed cell death. Numerous studies over the past 10 years indicate that prenatal and/or early postnatal ethanol exposure affects neurotransmitter-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 studies performed with experimental preparations from the brains of rodents exposed 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 investigations. Differences in ethanol exposure paradigms and blood alcohol concentrations obtained in these studies are highlighted, and directions for future research are suggested.
Results: Most studies have focused on the effects of prenatal or early postnatal ethanol exposure on NMDA receptors. These studies show that ethanol exposure affects ligand binding, subunit expression, and function of this receptor. Fewer studies have examined ethanol's effects on ligand-gated ion channels other than NMDA receptors. For instance, a study reported changes in ligand binding to hippocampal kainate receptors. Another study found alterations in modulation of GABA(A) receptors by benzodiazepines and neurosteroids.
Conclusions: These studies suggest that the effects of ethanol on brain ion channels may have a role in the pathophysiology of Alcohol-Related Neurodevelopmental Disorders and Fetal Alcohol Syndrome.