Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain
Abstract
The spinal cord dorsal horn (DH) integrates sensory processing but undergoes critical plasticity following nerve injury, leading to mechanical allodynia, or “touch-evoked pain”. It has been proposed that after nerve injury, innocuous sensory neurons gain access to nociceptive-specific (NS) circuits in the DH due to altered spinal inhibitory controls, thereby converting touch into pain. It is however unclear how sensory processing is reorganized under these conditions to generate this symptom. In this study, we used two-photon calcium imaging in mice to show that spinal disinhibition or nerve injury converts most DH excitatory neurons into highly polymodal cells, and unmasks an unprecedented number of previously silent neurons responding to a wide dynamic range (WDR) of sensory modalities. Using computational modeling, we further show that neuropathic pain likely does not result primarily from the transformation of excitatory NS neurons into WDR neurons, but rather from the activation of this previously dormant circuit.
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BibTeX
@article{negm2026sensory,
title = {{Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain}},
author = {Ahmed Negm and François Gabrielli and Mickael Zbili and Louis Poncet-Megemont and Karine Herault and Jennifer Makhoul and Anais Legrand and Philippe Luccarini and Alain Artola and Radhouane Dallel and Cedric Peirs},
journal = {Nature Communications},
year = {2026},
month = oct,
doi = {10.1038/s41467-026-76982-7},
url = {https://hal.science/hal-05782925v1},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Sensory plasticity of dorsal horn silent neurons as a critical mechanism for neuropathic pain
AU - Ahmed Negm
AU - François Gabrielli
AU - Mickael Zbili
AU - Louis Poncet-Megemont
AU - Karine Herault
AU - Jennifer Makhoul
AU - Anais Legrand
AU - Philippe Luccarini
AU - Alain Artola
AU - Radhouane Dallel
AU - Cedric Peirs
PY - 2026
DA - 2026/10/07
JO - Nature Communications
DO - 10.1038/s41467-026-76982-7
UR - https://hal.science/hal-05782925v1
AB - The spinal cord dorsal horn (DH) integrates sensory processing but undergoes critical plasticity following nerve injury, leading to mechanical allodynia, or “touch-evoked pain”. It has been proposed that after nerve injury, innocuous sensory neurons gain access to nociceptive-specific (NS) circuits in the DH due to altered spinal inhibitory controls, thereby converting touch into pain. It is however unclear how sensory processing is reorganized under these conditions to generate this symptom. In this study, we used two-photon calcium imaging in mice to show that spinal disinhibition or nerve injury converts most DH excitatory neurons into highly polymodal cells, and unmasks an unprecedented number of previously silent neurons responding to a wide dynamic range (WDR) of sensory modalities. Using computational modeling, we further show that neuropathic pain likely does not result primarily from the transformation of excitatory NS neurons into WDR neurons, but rather from the activation of this previously dormant circuit.
SN - 2041-1723
SN - 2041-1723
ER -