炎症に伴うin vivoラット脊髄後角への機械的感覚刺激に対する興奮性シナプス入力の増大

抄録

Tissue inflammation triggers either enhancement of nociceptive responses to mild noxious stimuli (hyperalgesia) or eliciting of pain in response to innoxious stimuli (allodynia). This hypersensitivity has been considered as sensitization of peripheral terminals of primary afferent or change in excitability of neurons in the spinal dorsal horn in activity dependent manner. In this study, how natural sensory synaptic inputs are transmitted from peripheral inflamed tissues to the superficial spinal dorsal horn was examined using in vivo patch-clamp recording techniques from substantia gelatinosa (SG, lamina II of the spinal cord) neurons and intracellular recording techniques from dorsal root ganglion neurons. In inflamed rats one to 4 days after inflammation, SG neurons exhibited spontaneous EPSCs with large amplitudes. The frequency of large amplitude of spontaneous and pinch-evoked EPSCs was much higher in inflamed than naive rats. The frequency of large amplitude of spontaneous EPSCs was decreased by topical application of NSAIDs to the inflamed skin. Although spontaneous firings were rarely observed in Aδ and C fibers in naive rats, about 50% of Aδ and C fibers generated APs spontaneously in inflamed rats. The population of C fibers having low mechanical threshold was increased in inflamed rats compared with naïve rats. The increased excitatory inputs in the SG due to sensitization of mechano-sensitive Aδ and C fibers may have an important role for the induction or development of plastic changes of spinal noxious circuits. [J Physiol Sci. 2008;58 Suppl:S134]