Research in the Gall laboratory has focused on circuit and synaptic mechanisms of learning and social behavior, and disturbances in these processes that arise in association with neuropsychiatric disorders and conditions of intellectual disability.  We have shown that disturbances in synaptic activity-regulated signaling to the actin cytoskeleton underlies learning impairments in animal models of the human conditions (Huntington’s Disease, Fragile X Syndrome (FXS), aging) and that natural neuromodulators can be exploited to enhance actin regulation and thereby restore synaptic plasticity and learning. This work has given rise to unexpected findings including the presence of sex differences in the synaptic receptors critical for hippocampus-dependent learning, and the required involvement of microglia and endocannabinoids for enduring synaptic plasticity in some projection systems. Current studies, using the rodent social isolation model to evaluate synaptic and circuit disturbances that contribute to depression, provide evidence that changes in activities of subpopulations of hippocampal interneurons contribute to depressive behavior. We are currently testing therapeutic approaches to enhance sociability and cognitive function, and to reduce signs of depression, in the different animal models.