INTRACELLULAR PHOSPHATIDYLINOSITOL PATHWAY ABNORMALITIES IN BIPOLAR DISORDER PATIENTS

A dysfunction in the intracellular signal transduction pathways may be implicated in the pathophysiology of bipolar disorder. In particular, the phosphatidylinositol (PI) signal transduction pathway may be a po ssible site of dysfunction. Platelets, peripheral cells, and post-mort em brain samples have been used as models in preliminary studies aimed at investigating this hypothesis. Emerging findings from clinical stu dies are consistent with a hyper-function in the PI pathway in the man ic state, which could be state-related. Findings of increased protein kinase C (PKC) activity in the manic state, and increased intracellula r Ca2+ responsiveness in the manic and possibly depressed states, are also consistent with a hyperactive PI pathway in this disorder. Future research should attempt to replicate and extend these preliminary fin dings further.