期刊
SCIENCE
卷 364, 期 6436, 页码 147-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aat8078
关键词
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资金
- Whitehall Foundation
- Hartwell Foundation
- One Mind Institute
- Rita Allen Foundation
- National Institute of Mental Health [R00 MH097822, R01 MH109685, R01 MH118451]
- Klingenstein-Simons Fellowship in Brain Science
- NSF
- KAKENHI [17H06312]
- CREST from JST [JPMJCR1652]
- SRPBS from AMED [17dm0107120h002]
- MEXT of Japan [26221001]
- WPI from MEXT of Japan
- Medical Scientist Training Program grant from the National Institute of General Medical Sciences of the National Institutes of Health [T32GM007739]
- NIH [F30 MH115622, R01 DA08259, HL136520]
- Simons Foundation [429965]
- Grants-in-Aid for Scientific Research [26221001] Funding Source: KAKEN
The neurobiological mechanisms underlying the induction and remission of depressive episodes over time are not well understood. Through repeated longitudinal imaging of medial prefrontal microcircuits in the living brain, we found that prefrontal spinogenesis plays a critical role in sustaining specific antidepressant behavioral effects and maintaining long-term behavioral remission. Depression-related behavior was associated with targeted, branch-specific elimination of postsynaptic dendritic spines on prefrontal projection neurons. Antidepressant-dose ketamine reversed these effects by selectively rescuing eliminated spines and restoring coordinated activity in multicellular ensembles that predict motivated escape behavior. Prefrontal spinogenesis was required for the long-term maintenance of antidepressant effects on motivated escape behavior but not for their initial induction.
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