ABSTRACT
Partial peripheral nerve injury occasionally results in neuropathic pain, including spontaneous burning pain and increased sensitivity to sensory stimuli such as hyperalgesia and allodynia. The pathophysiological mechanisms underlying this disease are poorly understood and the available treatments unsatisfactory. Presently, the neuropathic pain is believed to result from an increase in the excitability of the dorsal horn neurons (central sensitization), which is induced by abnormal signals from injured afferents. PKC-gamma is known to play a pivotal role in central sensitization following peripheral nerve injury. In the present study, we examine the expression of PKC-gamma mRNA of the spinal dorsal horn after neuropathic injury. There was no significant difference of PKC-gamma mRNA between lesion and control sides. These results suggest that PKC-gamma mRNA is not a key factor for the generation of neuropathic pain.