Abstract
Prenatal alcohol contributes to long-term learning disabilities, affecting 1/200 US live-births. In a model for fetal alcohol syndrome (FAS), we showed that alteration in NMDA receptors mediates adult alcohol-related learning deficit (Toso L AJOG2005). Alcohol is GABA-agonist and alcohol-induced inhibition of the excitatory NMDA may reduce activation of GABA inhibitory signals, resulting in uncontrolled firing at the synapse. GABA receptor subunit GABAAα5 is involved in spatial learning and is developmentally regulated, being excitatory in the perinatal brain and inhibitory in the adult.
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