Exposure to alcohol during pregnancy produces fetal alcohol spectrum disorders (FASD) which is associated with cognitive impairments in various neuropsychological domains. Children with FASD often exhibit sensorimotor dysfunctions that include deficits in motor coordination and fine motor control. Although developmental alcohol exposure has been shown to affect astrocytes and cause impairments in neuronal plasticity in several brain regions, very little is known about alterations in astrocytic Ca2+ signaling and synaptic changes that occur in the intact brain. Here we will use prenatal exposure mouse model of fetal alcohol spectrum disorders to study alcohol-induced alterations in basal and motor-skill learning induced astrocytic Ca2+ signaling and structural synaptic plasticity. We will combine in vivo imaging of dendritic spines with astrocytic Ca2+ imaging under basal conditions and with learning. The goal of the proposal is to determine whether developmental alcohol exposure results in alterations in basal and motor-skill learning induced astrocytic Ca2+ signaling and structural synaptic plasticity.
Children prenatally exposed to alcohol experience motor skill deficits. It is therefore important to determine the cellular mechanisms that govern motor learning in normal and developmentally abnormal brain. Here we will study the mechanism of motor learning in a mouse model of fetal alcohol spectrum disorders (FASD). We will test the hypothesis that prenatal exposure to alcohol alters astrocytic signaling resulting in synaptic impairments and motor learning deficits. Information about alterations in astrocytic signaling will help design therapeutic targets for treatment of FASD.
