Locus coeruleus-CA1 projections are involved in chronic depressive stress-induced hippocampal vulnerability to transient global ischaemia

Qian Zhang, Dian Xing Hu, Feng He, Chun Yang Li, Guang Jian Qi, Hong Wei Cai, Tong Xia Li, Jie Ming, Pei Zhang (), Xiao Qian Chen () and Bo Tian ()
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Qian Zhang: Huazhong University of Science and Technology
Dian Xing Hu: Huazhong University of Science and Technology
Feng He: Huazhong University of Science and Technology
Chun Yang Li: Huazhong University of Science and Technology
Guang Jian Qi: Huazhong University of Science and Technology
Hong Wei Cai: Huazhong University of Science and Technology
Tong Xia Li: Huazhong University of Science and Technology
Jie Ming: Huazhong University of Science and Technology
Pei Zhang: Huazhong University of Science and Technology
Xiao Qian Chen: Huazhong University of Science and Technology
Bo Tian: Huazhong University of Science and Technology

Nature Communications, 2019, vol. 10, issue 1, 1-17

Abstract: Abstract 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.

Date: 2019
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DOI: 10.1038/s41467-019-10795-9

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