Behavioral phenotypes are determined not only by the host genome, but by the hologenome, the combination of host and microbial genes. Gut microbiota are emerging as key regulators of both normal nervous system physiology and disease states. Working in the maternal high-fat diet model of autism, we recently identified a single bacterial species, Lactobacillus (L.) reuteri, which rescues social dysfunction and related deficits in social reward circuit plasticity. Specifically, we found that MHFD exposure induces long-term, functional changes in the offspring gut microbiome associated with dysregulation of the oxytocinergic system, deficits in social interaction-induced long-term plasticity in ventral tegmental area dopaminergic neurons, and resulting social impairments. Reconstitution with L. reuteri restored oxytocin levels, interaction-induced VTA plasticity, and social behavior in the offspring. In a follow-up study, we showed that L. reuteri rescues social dysfunction in multiple models of ASD of diverse pathoetiology (i.e., environmental, idiopathic, and genetic models) and that this rescue depends on vagus nerve integrity and oxytocin receptor signaling in dopaminergic neurons. Finally, I will present data from our ongoing investigation into how the MHFD-induced changes in the maternal gut microbiome alter maternal immune function and affect offspring brain development. Our findings identify the gut microbiome as a therapeutic target for neurodevelopmental disorders.