ABSTRACT
The catecholamine (CA) hypothesis of bipolar disorder (BD)—a deficiency of CA in depression and excess in mania-was proposed nearly three decades ago. CA abnormalities remain the most replicated finding in the pathophysiology of BD. However, the role of CA abnormalities in the pathophysiology of BD still remains unclear. For example, it is unclear whether changes in CAs seen in manic and depressed states are secondary to the mood state or primary, and it remains to be clarified whether abnormalities in CA system are presynaptic or postsynaptic. Rapid advances in the field of neuroscience in the last three decades have increased our knowledge of the role of CAs in the working of the nervous system and provided new tools to explore CA abnormalities. Clinical research in CA abnormalities in BD has evolved from measurement of changes in CAs in bodily fluids and peripheral tissue to neuroendocrine challenge studies to molecular analysis of postmortem tissue and direct visualization of CA system with brain imaging methods such as single photon emission computed tomography (SPECT) and positron emission tomography (PET).
