A Short Glance at the Neural Circuitry Mechanism Underlying Depression

Abstract

Depression leads to a large social burden because of its substantial impairment and disability in everyday activities. The prevalence and considerable impact of this disorder call for a better understanding of its pathophysiology to improve the diagnosis, treatment and prevention. Though productive animal models and pathophysiological theories have been documented, it is still very far to uncover the complex array of symptoms caused by depression. Moreover, the neural circuitry mechanism underlying behavioral changes in some depression-like behavior animals is still limited. Changes in the neural circuitry of amygdala, dorsal raphe nucleus, ventral tegmental area, hippocampus, locus coeruleus and nucleus accumbens are related to depression. However, the interactions between individual neural circuitry of different brain areas, have not yet been fully elucidated. The purpose of the present review is to examine and summarize the current evidence for the pathophysiological mechanism of depression, with a focus on the neural circuitry, and emphasize the necessity and importance of integrating individual neural circuitry in different brain regions to understand depression.

Abnormal GABAergic Neurotransmission in Depression

“…Depression as a neuropsychiatric disorder is characterized by anhedonia and lack of motivation [1], which has led to great social and economic burdens. A plethora of recent studies have highlighted the underlying mechanisms of this mood disorder from different aspects [2][3][4][5][6][7][8][9][10]. Generally, the pathogenesis of depression is closely associated with dysfunctions in neural circuits which, to some extent, are largely resulted from the abnormal neurotransmitter release from presynaptic neurons to their corresponding postsynaptic targets.…”