A Look Into the Dopamine Hypothesis for Bipolar Affective Disorder

The dopamine hypothesis in bipolar disorder (BD) has been a notable theory regarding the pathophysiology of manic and depressive phases of the disorder. There has been a greater use of antidopaminergics in treating BD, and there has been new in vivo neuroimaging and post-mortem studies. Researchers directed a systematic search for post-mortem, pharmacologic, functional magnetic resonance, and molecular imaging studies surrounding dopamine function through BD. It was found that the pharmacologic and imaging studies support the hypothesis that a state of hyperdopaminergia, particularly increases in D2/3 receptor availability and a hyperactive reward processing network, causes mania. The imaging studies of bipolar depression show heightened levels of dopamine transport, but other fluctuations of dopaminergic function were not consistent. The pharmacologic findings show that dopamine agonists and antidopaminergics may improve symptoms of bipolar depression. For the meantime, the researcher’s findings suggests a model where an increase in striatal D2/3 receptor accessibility would cause heightened dopaminergic neurotransmission and mania, while heightened levels of striatal dopamine transport would cause lessened dopaminergic function and depression. There are limitations to this model, but if it is confirmed, it can suggest new therapeutic strategies.

Reference: Ashok AH, Marques TR, Jauhar S, et al. The dopamine hypothesis of bipolar affective disorder: the state of the art and implications for treatment. Mol Psychiatry. 2017;22(5):666-679. doi:10.1038/mp.2017.16

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