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Nociceptors are excitatory neurons with free nerve endings that branch out from the axon and innervate parts of the dermis and epidermis. They are responsible for "translating" noxious signals into action potentials.
Some of the hallmarks of inflammatory pain are the decrease in the threshold to nociceptor activationn as well as the hypersensitization of the surrounding area even beyond the immediate site of inflammation (flare) to even innocuous stimuli (e.g. sensitivity to touch).
In the cellular level substance P and other neuropeptide release at the site of injury stimulate secretion of cytokines by resident immune cells (e.g. Langerhans and mast cells). These in turn cause vasodilation (reddening) and plasma extravasation (swelling). A large number of these secreted molecules also act directly or indirectly on nociceptor ion channels and receptors, resulting in hypersensitization.
This pathway card presents an overview of the cellular events at the injury site and the mechanisms of inflammatory nociceptor hypersensitization.