Effects of Developmental Alcohol Exposure on Primary and Associative Sensory Cortices

Individuals with fetal alcohol spectrum disorders (FASD) often present sensory alterations such as sensory overload, attention deficits, delayed auditory processing, and hypersensitivity to tactile stimulation. There is growing evidence showing that these sensory abnormalities give rise to social problems and learning deficits. Our lab has developed a ferret model of FASD that shows remarkable alterations in organization and plasticity of visual areas. For instance, alcohol exposure during the “third trimester” equivalent of human gestation reduces neuronal plasticity, decreases individual neuronal orientation tuning and disrupts the organization of orientation selectivity columns in the primary visual cortex. We propose that the sensory deficits caused by developmental alcohol exposure are not restricted to visual streams and that aberrant sensory responsiveness and disrupted integrative properties would also be seen in other sensory cortical areas. Here we test the hypothesis that abnormal refinement of cortical circuits caused by deficits in activity-neuronal plasticity caused by developmental alcohol exposure will dramatically affect cortical sensory processing. We will use a combination of in vivo electrophysiology and optical imaging of intrinsic signals to test our developmental alcohol exposures lead to synesthetic responses, with primary cortices displaying high responsivity to non-dominant sensory modalities (i.e. high responsivity to tactile stimulation in the auditory cortex); an alteration of tonotopic organization in auditory cortex and a disruption in multisensory integration in an auditory associative area. These experiments should make a major contribution to our understanding of sensory deficits in FASD.