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Functional coupling between peripheral nociceptor terminals in vivo is enhanced during acute inflammation
Devora Gershon1,2, Omer Barkai1,2,3, Nurit Engelmayer1,2
1Department of Medical Neurobiology; Institute for Medical Research Israel-Canada, The Hebrew University-Hadassah School of Medicine, Jerusalem, Israel.
Pain
|December 8, 2025
Summary
Activation of a single nociceptor terminal can trigger responses in neighboring unstimulated terminals via efferent signaling. This bidirectional communication contributes to the spread of hyperalgesia and inflammation beyond injured areas.
Area of Science:
- Neuroscience
- Immunology
- Pain Research
Background:
- Primary nociceptors transmit pain signals but also exhibit bidirectional communication.
- Peripheral nociceptor terminals release mediators influencing local immunity and inflammation.
- Previous studies linked phenomena to antidromic signaling, lacking direct evidence for efferent recruitment.
Purpose of the Study:
- To investigate efferent signaling from single nociceptor terminals.
- To determine if single nociceptor activation recruits neighboring unstimulated terminals.
- To explore the role of efferent signaling in acute hyperalgesia.
Main Methods:
- In vivo calcium imaging of individual nociceptive terminals in mouse corneas.
- Computational modeling to analyze signal propagation.
- Induction of acute hyperalgesia using proinflammatory cytokines.
Main Results:
- Single nociceptor terminal activation by capsaicin evoked responses in remote, unstimulated terminals.
- This efferent signaling depended on voltage-gated sodium and calcium channels.
- Proinflammatory cytokines enhanced efferent signaling and calcium signaling in remote terminals.
Conclusions:
- Demonstrated direct evidence of efferent signaling recruiting unstimulated nociceptor terminals.
- Identified enhanced efferent signaling in hyperalgesia, contributing to inflammation spread.
- Suggests intraterminal calcium increase drives mediator release, expanding hyperalgesia and inflammation.
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