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Pezawas, L., Meyer-Lindenberg, A., Drabant, E.M., Verchinski, B.A., Munoz, K.E., Kolachana, B.S., Egan, M.F., Mattay, V.S., Hariri, A.R. and Weinberger, D.R. (2005) 5-HTTLPR Polymorphism Impacts Human Cingulate-Amy- gdala Interactions: A Genetic Susceptibility Mechanism for Depression. Nature Neuroscience, 8, 828-834.
http://dx.doi.org/10.1038/nn1463

has been cited by the following article:

• TITLE: A Short Glance at the Neural Circuitry Mechanism Underlying Depression

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

  KEYWORDS: Pathophysiology, Depression-Like Behavior, Neural Circuitry

  JOURNAL NAME: World Journal of Neuroscience, Vol.6 No.3, June 16, 2016

  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.