期刊
SCIENCE
卷 366, 期 6469, 页码 1094-+出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aay8746
关键词
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资金
- European Research Council [ERC-2011-ADG-294313]
- National Research, Development and Innovation Office, Hungary [OTKA K119521, OTKA K115441, OTKA K109790, OTKA KH124345, OTKA NN125643, FK129019, PD121248, EFOP-3.6.3-VEKOP-16-2017-00009, NKFIH K120311, VKSZ_14-1-2O15-0155]
- U.S. National Institutes of Health [NS030549]
- Human Brain Project of the EU [EU H2020 720270]
- Hungarian Brain Research Program [2017-1.2.1-NKP-2017-00002]
- New National Excellence Program of the Ministry of Human Capacities, Hungary [UNKP-16-3-IV, UNKP-17-3-III-SE-9, UNKP-18-02-I-SE-20, UNKP-18-4-SE-126, UNKP-18-2-I-SE-22]
- Bolyai Janos Research Fellowship of the Hungarian Academy of Sciences
Adverse events need to be quickly evaluated and memorized, yet how these processes are coordinated is poorly understood. We discovered a large population of excitatory neurons in mouse median raphe region (MRR) expressing vesicular glutamate transporter 2 (vGluT2) that received inputs from several negative experience-related brain centers, projected to the main aversion centers, and activated the septohippocampal system pivotal for learning of adverse events. These neurons were selectively activated by aversive but not rewarding stimuli. Their stimulation induced place aversion, aggression, depression-related anhedonia, and suppression of reward-seeking behavior and memory acquisition-promoting hippocampal theta oscillations. By contrast, their suppression impaired both contextual and cued fear memory formation. These results suggest that MRR vGluT2 neurons are crucial for the acquisition of negative experiences and may play a central role in depression-related mood disorders.
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