posted on 2017-08-30, 00:00authored byGC Bristow, JA Bostrom, V. Haroutunian, MS Sodhi
GABAergic dysfunction has been strongly implicated in the pathophysiology of schizophrenia. In this study, we
analyzed the expression levels of several GABAergic genes in the anterior cingulate cortex (ACC) of postmortem
subjects with schizophrenia (n = 21) and a comparison group of individuals without a history of psychiatric illness
(n = 18). Our analyses revealed a significant sex by diagnosis effect, along with significant differences in
GABAergic gene expression based on medication status. Analyses revealed that in male groups, the expression
of GABAergic genes was generally lower in schizophrenia cases compared to the controls, with significantly
lower expression levels of GABA-Aα5, GABA-Aβ1, and GABA-Aε. In females, the expression of GABAergic genes
was higher in the schizophrenia cases, with significantly higher expression of the GABA-Aβ1 and GAD67
genes. Analysis of the effect of medication in the schizophrenia subjects revealed significantly higher expression
of GABA-Aα1-3, GABA-Aβ2, GABA-Aγ2, and GAD67 in the medicated group compared to the unmedicated group.
These data show that sex differences in the expression of GABAergic genes occur in the ACC in schizophrenia.
Therefore, our data support previous findings of GABAergic dysfunction in schizophrenia and emphasize the
importance of considering sex in analyses of the pathophysiology of schizophrenia. Sex differences in the
GABAergic regulation of ACC function may contribute to the differences observed in the symptoms of male and
female patients with schizophrenia. In addition, our findings indicate that antipsychotic medications may alter
GABAergic signaling in the ACC, supporting the potential of GABAergic targets for the development of novel antipsychotic medication.
Funding
This work was funded by the UIC Collaborative Engagement in Novel Therapeutic
Research and Enterprise award to MS, and NIH R01 awards MH066392 and MH064673
to VH.
History
Publisher Statement
This is the author’s version of a work that was accepted for publication in Schizophrenia Research. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Schizophrenia Research, DOI:10.1016/j.schres.2015.01.025