Abstract
Bipolar disorder (BD) is characterized by pathophysiological changes to the visceromotor network, disrupting the regulation of endocrine and autonomic responses to stress and, hence, emotion and behavior. Specifically, reductions in gray matter volume and/or cortical thickness and a concomitant increase in glutamatergic neurotransmission are observed in the pregenual (pgACC) and subgenual anterior cingulate cortex (sgACC); the orbitofrontal, frontal polar, and ventrolateral prefrontal cortex (PFC); and the posterior cingulate, ventral striatum, and hippocampus. Neuroreceptor imaging data provide preliminary evidence for serotonin, serotonin transporter (5-HTT), dopamine receptor, and cholinergic system dysfunction in BD. Recent PET imaging data also suggest microglial cell activation in mood disorders. Oft-reported abnormalities of the deep frontal and basal ganglia white matter, and enlargement of the third and lateral ventricles are likely associated with cerebrovascular disease. Mood stabilizers and antidepressant drugs may attenuate pathological limbic activity, increase neurotrophic processes, and decrease inflammation, restoring balance to the system.
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Savitz, J., Morris, H.M., Drevets, W.C. (2016). Neuroimaging Studies of Bipolar Depression: Therapeutic Implications. In: Zarate Jr., C., Manji, H. (eds) Bipolar Depression: Molecular Neurobiology, Clinical Diagnosis, and Pharmacotherapy. Milestones in Drug Therapy. Springer, Cham. https://doi.org/10.1007/978-3-319-31689-5_8
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