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Inflammatory pain forms part of nociception, the system of detection of harmful stimuli by the nervous system, which alerts the body to potential harm.
Inflammatory pain – an overview
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 activation as well as the hypersensitization of the surrounding area even beyond the immediate site of inflammation (flare) to even innocuous stimuli (eg sensitivity to touch).
At the cellular level, substance P and other neuropeptides released at the site of injury stimulate secretion of cytokines by resident immune cells (eg 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.
What to expect
This pathway poster presents an overview of the cellular events at the injury site and the mechanisms of inflammatory nociceptor hypersensitization.