期刊
NATURE COMMUNICATIONS
卷 10, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-019-10795-9
关键词
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资金
- National Natural Science Foundation of China [31371384, 31571044, 81471386, 81672504, 31600821]
- Programme for New Century Excellent Talents in University [NCET-10-0415]
- Integrated Innovative Team for Major Human Diseases Programme of Tongji Medical College, HUST [5001530026]
- China Postdoctoral Scientific Foundation [2015M582226, 2018T110774]
- Natural Science Foundation of Hubei Province [2017CFB465]
- Educational Commission of Hubei Province of China [D20182102]
- Fundamental Research Funds for the Central Universities [HUST: 2019kfyXJJS081]
Depression and transient ischaemic attack represent the common psychological and neurological diseases, respectively, and are tightly associated. However, studies of depression-affected ischaemic attack have been limited to epidemiological evidences, and the neural circuits underlying depression-modulated ischaemic injury remain unknown. Here, we find that chronic social defeat stress (CSDS) and chronic footshock stress (CFS) exacerbate CA1 neuron loss and spatial learning/memory impairment after a short transient global ischaemia (TGI) attack in mice. Whole-brain mapping of direct outputs of locus coeruleus (LC)-tyrosine hydroxylase (TH, Th:) positive neurons reveals that LC-CA1 projections are decreased in CSDS or CFS mice. Furthermore, using designer receptors exclusively activated by designer drugs (DREADDs)-based chemogenetic tools, we determine that Th:LC-CA1 circuit is necessary and sufficient for depression-induced aggravated outcomes of TGI. Collectively, we suggest that Th:LC-CA1 pathway plays a crucial role in depression-induced TGI vulnerability and offers a potential intervention for preventing depression-related transient ischaemic attack.
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