下眼窩神経損傷による痛覚過敏モデルにおける三叉神経脊髄路核のクロライド恒常性関連遺伝子発現変化

抄録

A loss of inhibition in the dorsal horn of the spinal cord is a crucial substrate for chronic pain syndromes. It involves a trans-synaptic reduction in the expression of the potassium-chloride exporter KCC2(Coull. et al. Nature 2003). We have prepared a rat experimental model of trigeminal neuropathic pain produced by a chronic constriction injury to the infraorbital nerve. By means of in situ hybridization histochemistry, we found that KCC2 mRNA was downregulated 1 to 3 weeks after ligation of the infraorbital nerve and it recovered after 4 weeks in the spinal trigeminal nucleus (Sp5). The time course of KCC2 mRNA downregulation and recovery was well correlated with the decrement and recovery of pain threshold to the mechanical stimuli. The KCC2 mRNA downregulation and recovery was also correlated with the increase and recovery of pain response. The result suggests that the KCC2 downregulation may play a role in the trigeminal neuralgia by impairing GABA inhibition which could be crucial for the analgesic action at the Sp5. [J Physiol Sci. 2007;57 Suppl:S143]