RT Journal Article
SR Electronic
T1 GABAergic malfunction underlying maternal immune activation-induced social deficits
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 319244
DO 10.1101/319244
A1 Kazuki Okamoto
A1 Natsuko Hitora-Imamura
A1 Hiroyuki Hioki
A1 Yuji Ikegaya
YR 2018
UL http://biorxiv.org/content/early/2018/05/10/319244.abstract
AB 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. 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.