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The mechanism of pain relief by low–power laser (Ga–Al–As diode laser, 16.2 mW) irradiation was studied using the patch–clamp technique in cultured mouse dorsal root ganglion neurons as sociated with C–fiber. Bradykinin (BK) and laser stimulation was limited to the process or the cell body using a specially developed separator. The action potentials of the cell body after BK application to the process were reversibly suppressed by 2 min irradiation of the process. K+ channel opening elicited by BK was reversibly suppressed by irradiation of the cell body. After irradiation of the cell body was performed without BK stimulation, the resting potential was depolarized by a potential of 2 – 3 mV, and the rate of the spike evoked by the depolarization pulse was increased. However, when irradiation was limited to the process, the rate of the spike was not increased. The inward current evoked by the depolarization pulse was not suppressed by irradiation of the cell body. BK–evoked inward currents evoked by BK application to the process were suppressed by irradiation of the process. When BK was applied to the process and irradiation of the cell body was performed, the BK–induced action potentials were not suppressed. When 1,2–dioctanoyl–sn–glycerol, a potent protein kinase C (PKC) activator, was applied concomitantly with BK to the process, the suppressive effects of laser irradiation were not observed. These results suggest that the increase in spike rate following the irradiation of the cell body without BK can be ascribed to depolarization due to inhibition of K+ channel opening, and the suppressive effects of laser irradiation on BK–evoked action potentials may come from suppression of the PKC–pathway in the process. Laser irradiation of the process is thus recommended for the treatment of BK–induced pain.

pain research

&lt;b&gt;Suppressive effects of low-power laser irradiation on bradykinin-induced action potentials in cultured &lt;/b&gt;&lt;b&gt;mouse dorsal root ganglion neurons &lt;/b&gt;