Divergent BLA engram circuits orchestrate social preference dynamics in bystander male mice with self-experienced stress
Abstract
Personal experiences are encoded and stored in memory engram cells and are crucial for social preference dynamics in future social contexts, yet the neural circuit mechanisms involved are still poorly understood. Here, we develop a mouse model that combines self-experienced single social defeat stress with vicarious social defeat stress, demonstrating a social preference with defeat stress-experienced cagemate and social avoidance toward an aggressor. Basolateral amygdala engram cells (BLA EC ) exhibit significant activation, and chemogenetic manipulations confirm their sufficiency and necessity for both social preference and social avoidance behaviors. Virus-based cell-type-specific brain mapping suggests BLA EC project to anterior cingulate cortex (ACC) and these projections are also responsible for modulating social preference dynamics. Distinct projections from BLA-ACC circuit, including ventral/dorsal hippocampus and zona incerta, exert the diverse effects on these behaviors in male mice. Our findings reveal regulation of social preference dynamics by divergent circuits originating from BLA EC , which may contribute to the neurobiological mechanism of social psychopathologies.
Article Details
Journal Info
Proceedings of the National Academy of Sciences
National Academy of Sciences
Authors (17)
Xue-Ke Yang
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Yu-Long Shi
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Ming Li
Tong-Xia Li
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Jian Yang
Jie Lei
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Chi Cui
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Xiang Peng
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Hong-Chu Zha
Hubei Provincial Clinical Research Center for Alzheimer’s Disease, Brain Science and Advanced Technology Institute, Tianyou Hospital, School of Medicine, Wuhan University of Science and Technology
Gan-Gan Luo
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Yi-Bo Yao
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Si-Tong Chen
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Jun-Song Du
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Hui-Juan Wang
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Shi-Qi Xu
Hubei Provincial Clinical Research Center for Alzheimer’s Disease, Brain Science and Advanced Technology Institute, Tianyou Hospital, School of Medicine, Wuhan University of Science and Technology
Pei Zhang
Department of Neurobiology, School of Basic Medicine, Tongji Medical College, Huazhong University of Science and Technology
Bo Tian
Hubei Provincial Clinical Research Center for Alzheimer’s Disease, Brain Science and Advanced Technology Institute, Tianyou Hospital, School of Medicine, Wuhan University of Science and Technology