Abstract
Fetal Alcohol Syndrome (FAS) is characterized by neurodevelopmental anomalies and life-long learning impairment. In a model for FAS we showed that prenatal treatment with neuroprotective peptides (NAP+SAL) prevented alcohol-induced learning deficits. We evaluated the role of GABA receptor as a potential mechanism for the peptide neuroprotection. The GABA-Aβ3 subunit is important for learning and is increased after alcohol exposure in the adult. We were interested in evaluating whether prenatal alcohol exposure affects GABA-Aβ3 and if the peptides mechanism of action for preventing alcohol-induced learning deficits includes the subunit.
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