ArticleeLife2025
A septo-hypothalamic-medullary circuit directs stress-induced analgesia.
Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Involvement of the hypothalamus-raphe magnus-spinal defecation center axis in stress-induced defecation in rats.Communications biology · 2026Article
- Lateral hypothalamus directs stress-induced modulation of acute and psoriatic itch.Cell reports · 2026Article
- Distinct lateral hypothalamus GABAergic projections regulate sensory and affective dimensions of pain.Zoological research · 2026Article
- Rostral Ventromedial Medulla (RVM) Projects to the Lateral Hypothalamic Area (LHA) to Drive Aversion and Anxiety.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026Article
- Effects of electroacupuncture at Zusanli on pain-perception-related brain nuclei in KOA mice: a study on cortical and subcortical c-fos expression.Behavioral and brain functions : BBF · 2026Article
- Lateral hypothalamic orexinergic neurons as central mediators of pain modulation and non-pharmacological analgesia.Frontiers in pharmacology · 2026Review
- Acute Restraint Stress and Pain Modulation Depend on the Interaction between the Periaqueductal Gray and the Lateral Septum.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
Stress is a potent modulator of pain. Specifically, acute stress due to physical restraint induces stress-induced analgesia (SIA). However, where and how acute stress and pain pathways interface in the brain are poorly understood. Here, we describe how the dorsal lateral septum (dLS), a forebrain limbic nucleus, facilitates SIA through its downstream targets in the lateral hypothalamic area (LHA) of mice. Taking advantage of transsynaptic viral-genetic, optogenetic, and chemogenetic techniques, we show that the dLS→LHA circuitry is sufficient to drive analgesia and is required for SIA. Furthermore, our results reveal that the dLS→LHA pathway is opioid-dependent and modulates pain through the pro-nociceptive neurons in the rostral ventromedial medulla (RVM). Remarkably, we found that the inhibitory dLS neurons are recruited specifically when the mice struggle to escape under restraint and, in turn, inhibit excitatory LHA neurons. As a result, the RVM neurons downstream of LHA are disengaged, thus suppressing nociception. Together, we delineate a poly-synaptic pathway that can transform escape behavior in mice under restraint to acute stress into analgesia.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.