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

J Neuroimmunol. 2018 Aug 15;321:92-96. doi: 10.1016/j.jneuroim.2018.06.006. Epub 2018 Jun 7.


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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Female
  • GABA Modulators / pharmacology
  • GABAergic Neurons / drug effects
  • GABAergic Neurons / immunology*
  • Gyrus Cinguli / drug effects
  • Gyrus Cinguli / immunology*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Organ Culture Techniques
  • Poly I-C / toxicity
  • Pregnancy
  • Prenatal Exposure Delayed Effects / chemically induced
  • Prenatal Exposure Delayed Effects / etiology
  • Prenatal Exposure Delayed Effects / metabolism*
  • Receptors, GABA-A / immunology*
  • Social Behavior*
  • Virus Diseases / chemically induced
  • Virus Diseases / complications
  • Virus Diseases / immunology*


  • GABA Modulators
  • Receptors, GABA-A
  • Poly I-C