ABSTRACT
BACKGREOUND: Capsaicin acts specifically on a subset of primary sensory neurons involved in nociception. In addition to its excitatory actions, capsaicin can have subsequent antinociception and anti-inflammatory effects due to pharmacological, functional desensitization and axonal degeneration. Because capsaicin has selective actions on unmyelinated C and thinly myelinated Adelta primary sensory neurons, it can be speculated that intrathecally adminstered capsaicin results prolonged analgesia without adverse effects related to the destruction of the nonnociceptive nerve fibers. METHODS: We performed experiments to investigate the effects of capsaicin on electrophysiological responses of acutely dissociated rat dorsal root ganglion neurons and pain-like behaviors, such as tail flick responses to hot water (53 degrees), formalin-induced hyperalgesic responses and allodynic responses induced by peripheral nerve injury. RESULTS: Capsaicin affects preferentially small- to medium-diameter rat dorsal root ganglion neurons. In capsaicin responsive cells, superfusion with capsaicin evoked membrane potential depolarization and large inward currents. Cellular excitablity was continuously suppressed even after 3 min wash-out. Intrathecally administered capsaicin had no effect on tail withdrawal latencies, but flinching responses induced by subcutaneous formalin and allodynic responses induced by peripheral nerve injury were suppressed by capsaicin. CONCLUSIONS: The results suggest that capsaicin which acts on primary sensory neurons carrying nociceptive information is effective in managing pain induced in a pathological condition, such as inflammatory and neuropathic pain. The data may also be applicable for seeking novel pharmacological strategies for managing intractable pain, i.e. chemical neurolysis.