دورية أكاديمية

A REM-active basal ganglia circuit that regulates anxiety.

التفاصيل البيبلوغرافية
العنوان: A REM-active basal ganglia circuit that regulates anxiety.
المؤلفون: Ba W; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Nollet M; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; UK Dementia Research Institute, Imperial College London, London SW7 2AZ, UK., Yin C; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; Department of Neonatal Medical Center, Children's Hospital of Nanjing Medical University, Nanjing 210000, China., Yu X; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Wong S; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; UK Dementia Research Institute, Imperial College London, London SW7 2AZ, UK., Miao A; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; UK Dementia Research Institute, Imperial College London, London SW7 2AZ, UK., Beckwith EJ; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Harding EC; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Ma Y; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Yustos R; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK., Vyssotski AL; Institute of Neuroinformatics, University of Zurich and ETH Zurich, Zurich 8057, Switzerland., Wisden W; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; UK Dementia Research Institute, Imperial College London, London SW7 2AZ, UK. Electronic address: w.wisden@imperial.ac.uk., Franks NP; Department of Life Sciences, Imperial College London, London SW7 2AZ, UK; UK Dementia Research Institute, Imperial College London, London SW7 2AZ, UK. Electronic address: n.franks@imperial.ac.uk.
المصدر: Current biology : CB [Curr Biol] 2024 Jun 25. Date of Electronic Publication: 2024 Jun 25.
Publication Model: Ahead of Print
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Cell Press Country of Publication: England NLM ID: 9107782 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-0445 (Electronic) Linking ISSN: 09609822 NLM ISO Abbreviation: Curr Biol Subsets: MEDLINE
أسماء مطبوعة: Publication: Cambridge, MA : Cell Press
Original Publication: London, UK : Current Biology Ltd., c1991-
مستخلص: Rapid eye movement (REM) sleep has been hypothesized to promote emotional resilience, but any neuronal circuits mediating this have not been identified. We find that in mice, somatostatin (Som) neurons in the entopeduncular nucleus (EP Som )/internal globus pallidus are predominantly active during REM sleep. This unique REM activity is both necessary and sufficient for maintaining normal REM sleep. Inhibiting or exciting EP Som neurons reduced or increased REM sleep duration, respectively. Activation of the sole downstream target of EP Som neurons, Vglut2 cells in the lateral habenula (LHb), increased sleep via the ventral tegmental area (VTA). A simple chemogenetic scheme to periodically inhibit the LHb over 4 days selectively removed a significant amount of cumulative REM sleep. Chronic, but not acute, REM reduction correlated with mice becoming anxious and more sensitive to aversive stimuli. Therefore, we suggest that cumulative REM sleep, in part generated by the EP → LHb → VTA circuit identified here, could contribute to stabilizing reactions to habitual aversive stimuli.
Competing Interests: Declaration of interests The authors declare no competing interests.
(Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.)
فهرسة مساهمة: Keywords: Vglut2 neurons; anxiety; basal ganglia; defensive behavior; emotion; habenula; non-rapid eye movement sleep; rapid eye movement sleep; somatostatin neurons; ventral tegmental area
تواريخ الأحداث: Date Created: 20240629 Latest Revision: 20240629
رمز التحديث: 20240630
DOI: 10.1016/j.cub.2024.06.010
PMID: 38944034
قاعدة البيانات: MEDLINE
الوصف
تدمد:1879-0445
DOI:10.1016/j.cub.2024.06.010