The interaction between α7nAChR and maternal infection in regulating schizophrenia- and autism-like behaviors
Wednesday, Nov 13, 2013, 11:00 AM -12:00 PM
++C.07.a. Autism: Genetic and animal models
, P. H. PATTERSON;
Div. of Biol., Caltech, Pasadena, CA
Microdeletion of human chromosome 15q13.3 increases the risk for autism and schizophrenia. One of the noteworthy genes in 15q13.3 is
, which encodes alpha7 nicotinic acetylcholine receptor (α7nAChR), which is associated with schizophrenia in clinical studies and in rodent models. We are investigating the interaction between α7nAChR and the environmental risk factor, maternal infection. The role of α7nAChR is being examined in two ways. First, we induce maternal immune activation (MIA) by maternal injection of poly(I:C) at mid-gestation, and test the effects of supplementing choline in the diet throughout embryonic and postnatal development until weaning, which would increase cholinergic signaling. Second, we test the behavior of MIA offspring in
mice. We find that maternal choline supplementation alleviates several schizophrenia- and autistic-like behaviors in MIA male offspring, such as deficits in sensory gating and social interaction, and, increased anxiety and repetitive behaviors. Moreover, compared to wild type mice, results with the
mice suggest that MIA increases sensory gating deficits. Thus, both perinatal environmental and genetic manipulations of α7nAChR can modulate the MIA-induced autistic/schizophrenia-like phenotype. One hypothesis to explain these results is that α7nAChR regulates the maternal inflammatory response to MIA.
NICOTINIC ACETYLCHOLINE RECEPTOR
MATERNAL IMMUNE ACTIVATION
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