Pain Matters: Nociceptive signaling drives neural encoding of inflammatory responses
- 1Tel Aviv University
Abstract
Pain is a cardinal sign of inflammation, constructed by the brain from peripheral nociceptive input. Yet, its role in the brain's response to inflammation remains unknown. Here, we demonstrate that nociceptive signaling is essential for the brain to represent and replay inflammatory states. Analysis of human fMRI and mouse activity mapping revealed that peripheral inflammation generates a distinct brain state. In mice, ablation of TRPV1+ sensory neurons or pharmacological analgesia disrupted this organization and prevented the insular cortex from forming retrievable immune representations. Conversely, augmenting nociceptive signaling during inflammation strengthened subsequent immune recall. These findings identify nociceptive input as a critical signal in brain-immune dialogue, enabling the encoding and retrieval of inflammatory events.
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BibTeX
@misc{sammons2026pain,
title = {{Pain Matters: Nociceptive signaling drives neural encoding of inflammatory responses}},
author = {M. Sammons and R. Assa Polansky and I. Zayalat and S. Breslauer Morris and L. Deng and H. Azulay-Debby and N. Singer and I. Chiu and A. Rolls},
howpublished = {bioRxiv},
year = {2026},
month = nov,
doi = {10.64898/2026.11.02.763662},
url = {https://www.biorxiv.org/content/10.64898/2026.11.02.763662v1},
note = {CC BY-NC-ND},
}
RIS
TY - UNPB
TI - Pain Matters: Nociceptive signaling drives neural encoding of inflammatory responses
AU - M. Sammons
AU - R. Assa Polansky
AU - I. Zayalat
AU - S. Breslauer Morris
AU - L. Deng
AU - H. Azulay-Debby
AU - N. Singer
AU - I. Chiu
AU - A. Rolls
PY - 2026
DA - 2026/11/02
PB - bioRxiv
DO - 10.64898/2026.11.02.763662
UR - https://www.biorxiv.org/content/10.64898/2026.11.02.763662v1
AB - Pain is a cardinal sign of inflammation, constructed by the brain from peripheral nociceptive input. Yet, its role in the brain's response to inflammation remains unknown. Here, we demonstrate that nociceptive signaling is essential for the brain to represent and replay inflammatory states. Analysis of human fMRI and mouse activity mapping revealed that peripheral inflammation generates a distinct brain state. In mice, ablation of TRPV1+ sensory neurons or pharmacological analgesia disrupted this organization and prevented the insular cortex from forming retrievable immune representations. Conversely, augmenting nociceptive signaling during inflammation strengthened subsequent immune recall. These findings identify nociceptive input as a critical signal in brain-immune dialogue, enabling the encoding and retrieval of inflammatory events.
ER -