@article{c02b23d4594542b69f5ef96a035df2c9,
title = "Role of Mesolimbic Brain-Derived Neurotrophic Factor in Depression",
abstract = "Brain-derived neurotrophic factor (BDNF) is widely accepted as being critical for neural and synaptic plasticity throughout the nervous system. Recent work has shown that BDNF in the mesolimbic dopamine (DA) circuit, originating in ventral tegmental area DA neurons that project to the nucleus accumbens, is crucial in the development of depressive-like behaviors following exposure to chronic social defeat stress in mice. Whereas BDNF modulates DA signaling in encoding responses to acute defeat stress, BDNF signaling alone appears to be responsible for the behavioral effects after chronic social defeat stress. Very different patterns are seen with another widely used chronic stress paradigm in mice, chronic mild stress (also known as chronic variable or unpredictable stress), where DA signaling, but not BDNF signaling, is primarily responsible for the behavioral effects observed. This review discusses the molecular, cellular, and circuit basis of this dramatic discrepancy, which appears to involve the nature of the stress, its severity and duration, and its effects on distinct cell types within the ventral tegmental area–to–nucleus accumbens mesolimbic circuit.",
keywords = "Animal models, BDNF, Chronic mild stress, Depression, Dopamine, Electrophysiology, Individual differences, Mesolimbic dopamine circuit, Nucleus accumbens, Social defeat stress, Ventral tegmental area",
author = "Koo, {Ja Wook} and Dipesh Chaudhury and Han, {Ming Hu} and Nestler, {Eric J.}",
note = "Funding Information: This work was supported by the Korea Brain Research Institute Basic Research Program (Grant No. 19-BR-02-05 [to JWK]), National Research Foundation of Korea funded by the Ministry of Science and ICT Brain Research Program and Biomedical Technology Development Program (Grant Nos. 2017M3C7A1048089 and 2018M3C7A1024150 [to JWK]), Brain and Behavior Research Foundation, New York University Research Challenge Fund (to DC), New York University Abu Dhabi Research Enhancement Fund (to DC), Al Jalila Research Foundation (to DC), National Institute of Mental Health (Grant Nos. R21MH112081 and R56MH115409 [to M-HH] and Grant Nos. R01MH051399 and P50MH096890 [to EJN]), National Institute of Alcohol Abuse (to M-HH), National Alliance for Research on Schizophrenia and Depression (to M-HH), and Hope for Depression Research Foundation (to EJN). The authors report no biomedical financial interests or potential conflicts of interest. Funding Information: This work was supported by the Korea Brain Research Institute Basic Research Program (Grant No. 19-BR-02-05 [to JWK]), National Research Foundation of Korea funded by the Ministry of Science and ICT Brain Research Program and Biomedical Technology Development Program (Grant Nos. 2017M3C7A1048089 and 2018M3C7A1024150 [to JWK]), Brain and Behavior Research Foundation , New York University Research Challenge Fund (to DC), New York University Abu Dhabi Research Enhancement Fund (to DC), Al Jalila Research Foundation (to DC), National Institute of Mental Health (Grant Nos. R21MH112081 and R56MH115409 [to M-HH] and Grant Nos. R01MH051399 and P50MH096890 [to EJN]), National Institute of Alcohol Abuse (to M-HH), National Alliance for Research on Schizophrenia and Depression (to M-HH), and Hope for Depression Research Foundation (to EJN). Publisher Copyright: {\textcopyright} 2019 Society of Biological Psychiatry",
year = "2019",
month = nov,
day = "15",
doi = "10.1016/j.biopsych.2019.05.020",
language = "English (US)",
volume = "86",
pages = "738--748",
journal = "Biological Psychiatry",
issn = "0006-3223",
publisher = "Elsevier USA",
number = "10",
}