Exposure to alcohol during pregnancy produces fetal alcohol spectrum disorders (FASD) that are associated with sensory and cognitive deficits. Individuals with FASD have impaired auditory processing and also frequently exhibit atypical auditory behaviors. Developmental alcohol exposure has been shown to cause impairments in neuronal plasticity including reduction in dendritic spines and alterations in AMPA receptor (AMPAR) function. However, currently there is a gap in understanding how the effects of alcohol on AMPARs alters synaptic plasticity in the intact brain and how changes in AMPAR trafficking can result in alterations in auditory processing. Here, we will use a prenatal exposure mouse model of FASD to investigate the mechanism of auditory processing deficits observed in FASD. We will examine auditory processing in mice prenatally exposed to alcohol, perform in vivo imaging in the primary auditory cortex to track AMPARs and dendritic spines over days, and perform electrophysiological recordings to study AMPAR-mediated synaptic transmission. The goal of the proposal is to provide a mechanistic basis for the altered auditory processing observed in FASD and examine the therapeutic potential of the BDNF mimetic 7,8-Dihydroxy flavone to preserve or restore central auditory processing following fetal alcohol exposure.