ArticleJCI insight2024
Distinct glutamatergic projections of the posteroventral medial amygdala play different roles in arousal and anxiety.
Article in JCI insight, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- The effect of Gua Sha therapy on Parkinson's disease with rapid eye movement sleep behavior disorder: a randomized controlled trial.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2025Trial
- Corticotropin-releasing hormone neurons in the bed nucleus of the stria terminalis control wakefulness in physiological and stressful conditions in mice.Molecular psychiatry · 2026Article
- Low-Frequency Stimulation at the Ventromedial Hypothalamus Exhibits Broad-Spectrum Efficacy Across Models of Epilepsy.CNS neuroscience & therapeutics · 2025Article
- Beta-Myrcene as a Sedative-Hypnotic Component from Lavender Essential Oil in DL-4-Chlorophenylalanine-Induced-Insomnia Mice.Pharmaceuticals (Basel, Switzerland) · 2024Article
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Authors and funding
15 authors.
Funding
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Abstract
Sleep disturbance usually accompanies anxiety disorders and exacerbates their incidence rates. The precise circuit mechanisms remain poorly understood. Here, we found that glutamatergic neurons in the posteroventral medial amygdala (MePVGlu neurons) are involved in arousal and anxiety-like behaviors. Excitation of MePVGlu neurons not only promoted wakefulness but also increased anxiety-like behaviors. Different projections of MePVGlu neurons played various roles in regulating anxiety-like behaviors and sleep-wakefulness. MePVGlu neurons promoted wakefulness through the MePVGlu/posteromedial cortical amygdaloid area (PMCo) pathway and the MePVGlu/bed nucleus of the stria terminals (BNST) pathway. In contrast, MePVGlu neurons increased anxiety-like behaviors through the MePVGlu/ventromedial hypothalamus (VMH) pathway. Chronic sleep disturbance increased anxiety levels and reduced reparative sleep, accompanied by the enhanced excitability of MePVGlu/PMCo and MePVGlu/VMH circuits but suppressed responses of glutamatergic neurons in the BNST. Inhibition of the MePVGlu neurons could rescue chronic sleep deprivation-induced phenotypes. Our findings provide important circuit mechanisms for chronic sleep disturbance-induced hyperarousal response and obsessive anxiety-like behavior and are expected to provide a promising strategy for treating sleep-related psychiatric disorders and insomnia.
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