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Stress-induced analgesia via supraspinal gate control
1Department of Neurology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei 230001, China.
Neuron
|June 17, 2026
Summary
Stress activates spinal GABAergic interneurons to reduce pain perception. These neurons, inhibited by the brainstem, are key to stress-induced analgesia and pain gating.
Area of Science:
- Neuroscience
- Pain Research
- Spinal Cord Function
Background:
- Stress-induced analgesia is a complex phenomenon involving descending pain modulation.
- The role of specific spinal interneurons in this process remains incompletely understood.
Purpose of the Study:
- To identify the specific spinal neuronal populations critical for stress-induced analgesia.
- To elucidate the mechanism by which stress modulates pain signaling at the spinal level.
Main Methods:
- Utilized genetic targeting of spinal GABAergic interneurons in mouse models.
- Employed behavioral assays to assess pain responses under stress conditions.
- Investigated neuronal activity and connectivity using in vivo and ex vivo techniques.
Main Results:
- Identified spinal GABAergic interneurons as essential mediators of stress-induced analgesia.
- Demonstrated that these interneurons receive tonic inhibitory control from the rostral ventromedial medulla.
- Showed that stress leads to the disinhibition of these interneurons, facilitating pain gate closure.
Conclusions:
- Spinal GABAergic interneurons act as a critical node in the stress-induced analgesia pathway.
- Disinhibition of these neurons by stress provides a novel mechanism for spinal pain gating.
- Findings offer new insights into the neurobiology of pain modulation and potential therapeutic targets.
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