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Background  Pre-mRNAs of 2-amino-3-(3-hydroxy-5-methyl-isoxazol-4-yl)-propanoic acid (AMPA)/kainate glutamate receptors undergo post-transcriptional modification known as RNA editing that is mediated by adenosine deaminase acting on RNA type 2 ( ADAR2 ). This modification alters the amino acid sequence and function of the receptor. Glutamatergic signaling has been suggested to have a role in mood disorders and schizophrenia, but it is unknown whether altered RNA editing of AMPA/kainate receptors has pathophysiological significance in these mental disorders. In this study, we found that  ADAR2  expression tended to be decreased in the postmortem brains of patients with schizophrenia and bipolar disorder.    Results  Decreased  ADAR2  expression was significantly correlated with decreased editing of the R/G sites of AMPA receptors. In heterozygous  Adar2  knockout mice ( Adar2  +/−  mice), editing of the R/G sites of AMPA receptors was decreased.  Adar2  +/−  mice showed a tendency of increased activity in the open-field test and a tendency of resistance to immobility in the forced swimming test. They also showed enhanced amphetamine-induced hyperactivity. There was no significant difference in amphetamine-induced hyperactivity between  Adar2  +/−  and wild type mice after the treatment with an AMPA/kainate receptor antagonist, 2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo[f]quinoxaline.    Conclusions  These findings collectively suggest that altered RNA editing efficiency of AMPA receptors due to down-regulation of  ADAR2  has a possible role in the pathophysiology of mental disorders.

A role of ADAR2 and RNA editing of glutamate receptors in mood disorders and schizophrenia