A Short Glance at the Neural Circuitry Mechanism Underlying Depression

Chanyi Lu,Yaoyao Li,Qiqin Li,Yun-Feng Zhang,Yun Wang

doi:10.4236/wjns.2016.63023

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.

Highlights

Depression is a heterogeneous symptom complex, characterized by an overwhelming sense of fatigue, neuropsychiatric and vegetative symptoms, neuroimmunological disturbances [1], neuroendocrine abnormalities, and some other somatic complaints [2]
A possible role of the mPFC-dorsal raphe nucleus (DRN) neural circuitry in depression has been confirmed by the fact that the stimulation of axons of the medial prefrontal cortex neurons in the DRN increased swimming behavior during the forced swimming test (FST) [24]
The disruption of firing properties of individual neurons or synaptic plasticity caused by antidepressants will affect neural circuitry related to depression [28]. It implies that both the intrinsic electrophysiological properties of the DRN serotonergic neurons and the neural circuitry formed between DRN and other brain areas are involved in depression

Summary

Introduction

Depression is a heterogeneous symptom complex, characterized by an overwhelming sense of fatigue, neuropsychiatric and vegetative symptoms, neuroimmunological disturbances [1], neuroendocrine abnormalities, and some other somatic complaints [2]. Our ongoing study suggested that the neural circuitry in both intrinsic electrophysiological and synaptic connection properties of pyramidal neurons changed significantly in the depression-like behavior mouse model. The role of neural circuitry between amygdala and other cerebral cortex areas has been identified an abnormal connectivity for each voxel in the whole brain of patients with depression.

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Conclusion