GABAergic malfunction in the anterior cingulate cortex underlying maternal immune activation-induced social deficits.

J Neuroimmunol. 2018 Aug 15;321:92-96

Authors: Okamoto K, Hitora-Imamura N, Hioki H, Ikegaya Y

Abstract
Social deficits are one of the major symptoms of psychiatric disorders, including autism spectrum disorders (ASDs) and schizophrenia. However, the underlying mechanism remains ill-defined. Here, we focused on the anterior cingulate cortex (ACC), a brain region that is related to social behaviors, of mice that received poly(I:C)-induced maternal immune activation. Offspring born from poly(I:C)-treated dams exhibited social deficits in a three-chamber task at juvenile stages. Using whole-cell patch clamp recordings, we found that layer 2/3 pyramidal cells were hyperactive in acute ACC slices prepared from poly(I:C)-treated mice compared to those from saline-treated mice. The hyperexcitation was associated with a reduction in inhibitory synapse activity. Local injection of the GABAA receptor enhancer clonazepam into the ACC of poly(I:C)-treated mice restored the social behaviors of the mice. These results suggest that the balanced excitability of ACC neurons is essential for social ability.

PMID: 29957393 [PubMed – in process]

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