Abstract

One of the concepts that makes pediatric psychiatry complex is the interaction of the developing neurological system and mental illnesses. Specifically, inhibitory neuron development must be understood because GABAergic abnormalities have been implicated in the pathogenesis of autism spectrum disorder (ASD), schizophrenia, and Tourette’s disorder. By use of mouse models, our laboratory has found that prenatal stress alters GABAergic neurons, particularly the parvalbumin (PV) subtype, in the medial frontal cortex and hippocampus. We also found that prenatal stress increases anxiety-like behavior and decreases social preference in mice, alterations correlated with inhibitory neuron abnormalities, and mirroring neuropsychiatric symptoms. Thus, if GABAergic neuron changes after prenatal stress could be rescued, this might contribute to the prevention of mental illness. GABAergic neurons are sensitive to oxidative stress, a possible mechanism of prenatal stress, suggesting that the antioxidant N-acetylcysteine (NAC) could rescue GABAergic neuron changes.

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