Increased G alpha(q/11) immunoreactivity in postmortem occipital cortex from patients with bipolar affective disorder

As disturbances in guanine nucleotide binding (G) protein-coupled phosphoinositide second messenger systems have been implicated in bipolar disorder, we examined whether the abundance of G alpha(q/11) and phospholipase C (PLC)-beta(1) two key transducing proteins in this signaling pathway, are altered in this disorder, Compared with the controls, immunoreactive levels of G alpha(q/11) were significantly elevated by 62% (p = .047) in occipital cortex of bipolar subjects. A similar increase (52%) in the PLC-beta(1) immunolabeling was also found in the occipital cortex of the bipolar subjects, but only reached marginal statistical significance (p = .07). In contrast, frontal and temporal cortex G(alpha/11) or PLC-beta(1) immunolabeling did not differ between bipolar and control subjects. Cerebral cortical immunoreactive levels of G beta(1) or G beta(2), included as a negative control, were not different between comparison groups. These findings support and extend earlier observations suggesting that disturbances in G protein-coupled second messenger signaling pathways may play an important role in the pathophysiology of bipolar affective disorder. (C) 1997 Society of Biological Psychiatry.