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A common thalamic hub for general and defensive arousal control.
Wang, Yiwei; You, Ling; Tan, KaMun; Li, Meijie; Zou, Jingshan; Zhao, Zhifeng; Hu, Wenxin; Li, Tianyu; Xie, Fenghua; Li, Caiqin; Yuan, Ruizhi; Ding, Kai; Cao, Lingwei; Xin, Fengyuan; Shang, Congping; Liu, Miaomiao; Gao, Yixiao; Wei, Liqiang; You, Zhiwei; Gao, Xiaorong; Xiong, Wei; Cao, Peng; Luo, Minmin; Chen, Feng; Li, Kun; Wu, Jiamin; Hong, Bo; Yuan, Kexin.
Affiliation
  • Wang Y; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • You L; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Tan K; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Li M; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Zou J; Hospital of Chengdu University of Traditional Chinese Medicine, Traditional Chinese Medicine Hospital of Sichuan Province, Chengdu 610036, China.
  • Zhao Z; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; Department of Automation, Tsinghua University, Beijing 100084, China.
  • Hu W; School of Aerospace Engineering, Tsinghua University, Beijing 100084, China.
  • Li T; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Xie F; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; Tsinghua Laboratory of Brain and Intelligence (THBI), Beijing 100084, China.
  • Li C; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Yuan R; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China.
  • Ding K; Department of Chemical Engineering, Tsinghua University, Beijing 100084, China.
  • Cao L; Zhili College, Tsinghua University, Beijing 100084, China.
  • Xin F; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China.
  • Shang C; National Institute of Biological Sciences (NIBS), Beijing 102206, China.
  • Liu M; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; Laboratory Animal Resources Center, Tsinghua University, Beijing 100084, China.
  • Gao Y; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Joint Center for Life Sciences, Beijing 100084, China.
  • Wei L; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; School of Life Sciences, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Joint Center for Life Sciences, Beijing 100084, China.
  • You Z; Department of Basic Medical Sciences, School of Medicine, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Joint Center for Life Sciences, Beijing 100084, China; Laboratory of Dynamic Immunobiology, Institute for Immunology, Tsinghua University, Beijing 100084, China.
  • Gao X; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; Tsinghua Laboratory of Brain and Intelligence (THBI), Beijing 100084, China.
  • Xiong W; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; School of Life Sciences, Tsinghua University, Beijing 100084, China; Chinese Institute for Brain Research, Beijing 102206, China.
  • Cao P; National Institute of Biological Sciences (NIBS), Beijing 102206, China.
  • Luo M; National Institute of Biological Sciences (NIBS), Beijing 102206, China; Chinese Institute for Brain Research, Beijing 102206, China.
  • Chen F; Department of Automation, Tsinghua University, Beijing 100084, China.
  • Li K; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; School of Life Sciences, Tsinghua University, Beijing 100084, China; Tsinghua-Peking Joint Center for Life Sciences, Beijing 100084, China.
  • Wu J; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; Department of Automation, Tsinghua University, Beijing 100084, China.
  • Hong B; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; Tsinghua Laboratory of Brain and Intelligence (THBI), Beijing 100084, China. Electronic address: hongbo@mail.tsinghua.edu.cn.
  • Yuan K; Department of Biomedical Engineering, School of Medicine, Tsinghua University, Beijing 100084, China; IDG/McGovern Institute for Brain Research at Tsinghua, Beijing 100084, China; Tsinghua Laboratory of Brain and Intelligence (THBI), Beijing 100084, China. Electronic address: kexinyuan@mail.tsinghua
Neuron ; 111(20): 3270-3287.e8, 2023 10 18.
Article in En | MEDLINE | ID: mdl-37557180
ABSTRACT
The expression of defensive responses to alerting sensory cues requires both general arousal and a specific arousal state associated with defensive emotions. However, it remains unclear whether these two forms of arousal can be regulated by common brain regions. We discovered that the medial sector of the auditory thalamus (ATm) in mice is a thalamic hub controlling both general and defensive arousal. The spontaneous activity of VGluT2-expressing ATm (ATmVGluT2+) neurons was correlated with and causally contributed to wakefulness. In sleeping mice, sustained ATmVGluT2+ population responses were predictive of sensory-induced arousal, the likelihood of which was markedly decreased by inhibiting ATmVGluT2+ neurons or multiple downstream pathways. In awake mice, ATmVGluT2+ activation led to heightened arousal accompanied by excessive anxiety and avoidance behavior. Notably, blocking their neurotransmission abolished alerting stimuli-induced defensive behaviors. These findings may shed light on the comorbidity of sleep disturbances and abnormal sensory sensitivity in specific brain disorders.
Subject(s)
Key words

Full text: 1 Database: MEDLINE Main subject: Arousal / Thalamus Type of study: Prognostic_studies Language: En Journal: Neuron Year: 2023 Type: Article Affiliation country: China

Full text: 1 Database: MEDLINE Main subject: Arousal / Thalamus Type of study: Prognostic_studies Language: En Journal: Neuron Year: 2023 Type: Article Affiliation country: China