Acute noxious heat pain
Nowadays, one cannot but recognize a key role of the peripheral and central glial cells for generation of clinical neuropathic pain. Many cytokines are released from glial cells, immune cells and nociceptive primary afferent central or peripheral terminals by injury, bacterial or viral infection, and envenomation by bee venom or scorpion. Released cytokines mutually affect by paracrine or autocrine manner among glias, immune cells and neurons, thereby produce and transmit the exaggerating pain information to the brain. Indeed, suppression of activated glia and immune cells by chemical agents or antibodies can relief abnormal pain caused by various experimental neuropathies. Thus, abnormal exaggerated pain cannot be explained without the role of glia and immune cells. Many investigators emphasized that therapeutic use of inactivating agents to glial and immune cells but not to neurons is available for alleviation of clinical pain. Thermo-TRP channels, TRPV1, TRPA1 and TRPM8 could not sense neuropathic pain by themselves without close interactions between glias, immune cells and TRP channels. The removal of persistent clinical pain will be rescued by treatment with inactivating chemicals to glias and immune cells. In addition, physiological noxious heat could be sensed by unknown sensor other than thermo-TRP channels, TRPV1, TRPA1 and TRPM8
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