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 phos phoinositide second messenger systems have been implicated in bipolar disorder, we examined whether the abundance of G alpha(q/11) and phosp holipase C (PLC)-beta(1) two key transducing proteins in this signalin g pathway, are altered in this disorder, Compared with the controls, i mmunoreactive levels of G alpha(q/11) were significantly elevated by 6 2% (p = .047) in occipital cortex of bipolar subjects. A similar incre ase (52%) in the PLC-beta(1) immunolabeling was also found in the occi pital cortex of the bipolar subjects, but only reached marginal statis tical significance (p = .07). In contrast, frontal and temporal cortex G(alpha/11) or PLC-beta(1) immunolabeling did not differ between bipo lar and control subjects. Cerebral cortical immunoreactive levels of G beta(1) or G beta(2), included as a negative control, were not differ ent between comparison groups. These findings support and extend earli er observations suggesting that disturbances in G protein-coupled seco nd messenger signaling pathways may play an important role in the path ophysiology of bipolar affective disorder. (C) 1997 Society of Biologi cal Psychiatry.