Abstract
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 behavioural symptoms during episodes of fever, a sign of systemic inflammation. However, a mechanistic understanding of how fever-associated immune responses translate into behavioural relief—both at the molecular and neural level—is lacking. We show that the social behavioural deficits in offspring exposed to maternal immune activation can be temporarily rescued by the inflammatory response elicited by the administration of lipopolysaccharide (LPS). This behavioural 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 behavioural phenotypes associated with offspring exposed to MIA. We also show that both the behavioural 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.
Biography:
Gloria Choi is an investigator at the Picower Institute for Learning and Memory and an associate professor in the Department of Brain and Cognitive Sciences at the Massachusetts Institute of Technology. She received her undergraduate degree from the University of California, Berkeley. Choi completed her Ph.D. at the California Institute of Technology where she worked in the laboratory of David Anderson. She was a postdoctoral research scientist in the laboratory of Richard Axel at Columbia University. Choi’s lab studies the interaction of the immune system with the brain and the effects of that interaction on neurodevelopment, neural circuit function and behaviour.
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