Nociceptors: thermal allodynia and thermal pain

The sensation of pain plays a vital protecting role, alerting organisms about potentially damaging stimuli. Tissue injury is detected by nerve endings of specialized peripheral sensory neurons called nociceptors that are equipped with different ion channels activated by thermal, mechanic, and chemical stimuli. Several transient receptor potential channels have been identified as molecular transducers of thermal stimuli in pain-sensing neurons. Skin injury or inflammation leads to increased sensitivity to thermal and mechanic stimuli, clinically defined as allodynia or hyperalgesia. This hypersensitivity is also characteristic of systemic inflammatory disorders and neuropathic pain conditions. Mechanisms of thermal hyperalgesia include peripheral sensitization of nociceptor afferents and maladaptive changes in pain-encoding neurons within the central nervous system. An important aspect of pain management involves attempts to minimize the development of nociceptor hypersensitivity. However, knowledge about the cellular and molecular mechanisms causing thermal hyperalgesia and allodynia in human subjects is still limited, and such knowledge would be an essential step for the development of more effective therapies.