The biological basis of bipolar disorder is not known. Models for the illness have been proposed that were based on the neurobiological effects of pharmacological agents that affect mood. Although of great interest, these models have not adequately explained the striking clinical pattern of illness in which patients may experience either unipolar episodes or bipolar cycles of mania and depression. We now present a new model suggesting that the unique clinical heterogeneity found in patients with bipolar disorder could be explained by a defect in a 'downstream' portion of a signal transduction pathway that can regulate two or more neurotransmitter systems that have opposite effects on neuronal activity. This model may target specific candidate genes for involvement in bipolar disorder.
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