Injury-induced nociceptive pain sensitization is a normal response to injury: the nociceptive threshold for pain is reduced (allodynia) and an increased pain signal is produced (hyperalgesia). However, if the response persists after the injury is healed, chronic pain can result.
Injury-induced nociceptive pain sensitization has been characterized in multiple studies in Drosophila. Ultraviolet (UV) irradiation is typically used to induce tissue damage, usually in third instar larvae. Thermal (heat) nociception assays are most common; response to mechanical force has also been used. Several molecular pathways involved in the pain sensitization response have been investigated. Work in flies has allowed investigation of allodynia and hyperalgesia as separable responses.
[updated Oct. 2021 by FlyBase; FBrf0222196]
When an injury occurs the nociceptive threshold for pain is reduced (allodynia) and an increased pain signal is produced (hyperalgesia); this fosters behavior that protects damaged tissue during healing. Sensitization normally subsides after the injury is healed, however, dysregulation can occur which results in sensitization that persists after the injury has healed and can result in chronic pain (FBrf0250205 and references cited therein).
Nociceptors are sensory end organs in the skin, muscle, joints and viscera that selectively respond to noxious or potentially tissue-damaging stimuli. Pain usually starts with the activation of nociceptors, which convey nociceptive (pain) information to the CNS. An important property of nociceptors is that they sensitize (that is, their excitability can be increased). Sensitization, which typically develops as a consequence of tissue insult and inflammation, is defined as a reduction in the threshold and an increase in the magnitude of a response to noxious stimulation. (Gold and Gebhart, 2010; pubmed:20948530).