期刊
SCIENCE
卷 351, 期 6268, 页码 -出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aac9698
关键词
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资金
- Defense Advanced Research Projects Agency Neuro-FAST program
- National Institute of Mental Health
- National Institute on Drug Abuse (NIDA)
- NSF
- Simons Foundation
- Gatsby Foundation
- Wiegers Family Fund
- Grosfeld Foundation
- Reeves Foundation
- Snyder Foundation
- Woo Foundation
- Albert Yu and Mary Bechman Foundation
- NIH [P41 EB015891, R00 MH097822]
- Bio-X Seed grant
- Stanford Neuroscience Institute
- Fulbright International Science and Technology Fellowship
- Stanford Graduate Fellowship
- Gerald J. Lieberman Fellowship
- Stanford Neurosciences Program NIH Training Grant
- National Research Service Award Predoctoral Fellowship from NIDA [1F31MH105151_01]
- NARSAD
- NATIONAL INSTITUTE OF BIOMEDICAL IMAGING AND BIOENGINEERING [P41EB015891] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [F31MH105151, R01MH086373, DP2MH109982, R00MH097822, F30MH010515] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [R37DA035377] Funding Source: NIH RePORTER
Motivation for reward drives adaptive behaviors, whereas impairment of reward perception and experience (anhedonia) can contribute to psychiatric diseases, including depression and schizophrenia. We sought to test the hypothesis that the medial prefrontal cortex (mPFC) controls interactions among specific subcortical regions that govern hedonic responses. By using optogenetic functional magnetic resonance imaging to locally manipulate but globally visualize neural activity in rats, we found that dopamine neuron stimulation drives striatal activity, whereas locally increased mPFC excitability reduces this striatal response and inhibits the behavioral drive for dopaminergic stimulation. This chronic mPFC overactivity also stably suppresses natural reward-motivated behaviors and induces specific new brainwide functional interactions, which predict the degree of anhedonia in individuals. These findings describe a mechanism by which mPFC modulates expression of reward-seeking behavior, by regulating the dynamical interactions between specific distant subcortical regions.
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