Abstract
Trigeminal neuralgia is one of the most common chronic pain syndromes, of which animal model has not been established and etiology is still unknown. We have developed a rat model of trigeminal hyperalgesia produced by a chronic constrictive injury with ligation of the infraorbital nerve. Pain threshold and the pain response scores to the mechanical stimulation were determined in the receptive-field by comparing sham-operated and injured sides. The pain threshold was reduced and the pain response score increased from 1 to 3 weeks and then recovered 4 weeks after injury. By means of in situ hybridization and immunohistochemistry, we found that the Cl- -extruder KCC2 mRNA and protein were downregulated in secondary neurons in injury side of spinal trigeminal nucleus (Sp5). The Cl- importer NKCC1 mRNA was upregulated in the small-sized and large-sized primary neurons in the injured side of the trigeminal ganglion (TG). These significant downregulation of KCC2 and significant upregulation of NKCC1 were observed from 1 to 2 weeks after injury. The results suggest that NKCC1 upregulation in TG may facilitate pain conduction and transmission by autocrine and presynaptic GABAergic depolarizations, respectively. KCC2 downregulation in Sp5 may result in disinhibition by impairing GABA inhibition. Such Cl- homeostatic disruption may increase pain transmission which may underlie the pathophysilology of the trigeminal neuralgia. [J Physiol Sci. 2008;58 Suppl:S151]
