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Notably, dysfunction of GABAergic inhibitory interneurons induced a glutamate storm from excitatory glutamatergic cortical pyramidal neurons and a hyperdopaminergic subcortical state [35], corroborating the hypothesis that prenatal exposure to inflammation would result in an altered gene expression profile in the hippocampal structures and disruption in GABAergic, glutamatergic, and serotonergic neuronal circuits relevant to a model of inflammation-mediated psychosis [53,73,74]
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