Pain Matters: Nociceptive signaling drives neural encoding of inflammatory responses
Auteurs : M. Sammons, R. Assa Polansky, I. Zayalat, S. Breslauer Morris, L. Deng, H. Azulay-Debby, N. Singer, I. Chiu, A. Rolls
Résumé scientifique
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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Résumé scientifique
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Résumé scientifique
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Résumé scientifique
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Résumé scientifique
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Les travaux antérieurs sur lesquels il s’appuie
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Résumé scientifique
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Résumé scientifique
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Résumé scientifique
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Résumé scientifique
In the 1990s, the identification of a non-selective ion channel, especially responsive to capsaicin, revolutionized the studies of somatosensation and pain that were to follow. The TRPV1 channel is expressed mainly in neuronal cells, more specifically, in sensory neurons responsible for the perception of noxious stimuli. However, its presence has also been detected in other non-neuronal cells, such as immune cells, β- pancreatic cells, muscle cells and adipocytes. Activation of the channel occurs in response to a wide range of stimuli, such as noxious heat, low pH, gasses, toxins, endocannabinoids, lipid-derived endovanilloid, and chemical agents, such as capsaicin and resiniferatoxin. This …
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