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The beneficial effects of infection and the ensuing inflammation on neurological disorders have previously been noted. For example, a subset of children with autism spectrum disorder (ASD) exhibits temporary but considerable improvements in their behavioral symptoms during episodes of fever, a sign of systemic inflammation. However, a mechanistic understanding of how fever-associated immune responses translate into behavioral relief鈥攂oth at the molecular and neural level鈥攊s lacking. We show that the social behavioral deficits in offspring exposed to maternal immune activation can be temporarily rescued by the inflammatory response elicited by the administration of lipopolysaccharide (LPS). This behavioral rescue was accompanied by a reduction in neural activity in the primary somatosensory cortex dysgranular zone (S1DZ), the hyperactivity of which has previously been implicated in the manifestation of behavioral phenotypes associated with offspring exposed to MIA. We also show that both the behavioral rescue and the reduction in neural activity are mediated through the expression of IL-17 receptor subunit a (IL-17Ra) in the neurons of the S1DZ.

This seminar will be given online via Zoom. Details in attached poster.