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 possible site of dysfunction. Platelets, peripheral cells, and post-mortem brain samples have been used as models in preliminary studies aimed at investigating this hypothesis. Emerging findings from clinical studies are consistent with a hyperfunction in the PI pathway in the manic state, which could be state-related. Findings of increased protein kinase C (PKC) activity in the manic state, and increased intracellular 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 findings further.
Soares
J C
JC
Department of Psychiatry, Western Psychiatric Institute and Clinic, University of Pittsburgh School of Medicine, PA, USA.
Mallinger
A G
AG
D001714:Bipolar Disorder / Q000378:metabolism*; D001792:Blood Platelets / Q000378:metabolism; D001921:Brain / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D006801:Humans; D010716:Phosphatidylinositols / Q000378:metabolism*; D011493:Protein Kinase C / Q000378:metabolism; D015398:Signal Transduction
D010716:Phosphatidylinositols; D011493:Protein Kinase C; D002118:Calcium