Glutamate receptor antagonist reduces pain following experimental tooth movement

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Various studies reported c-Fos expression in the neurons in the trigeminal sensory nuclear complex (TSNC) following experimental tooth movement, which implies pain transmission to the central nervous system. Meanwhile, MK-801, a non-competitive antagonist of N-methyl-D-aspartate (NMDA) receptors, was shown to markedly reduce the expression of c-Fos in the trigeminal subnucleus caudalis (Vc) following noxious stimulation, but to enhance c-Fos expression markedly in other brain regions, i.e., the neocortex, dorsal raphe and thalamic nuclei. In the present study, we examined the nature of c-Fos expression in the brainstem including the TSNC and mid-brain following administration of MK-801 and/or experimental movement of the rat molars. Twelve hours after the beginning of experimental tooth movement, c-Fos was expressed bilaterally in the superficial laminae of Vc (Vc I/II), dorsomedial areas of the trigeminal subnucleus oralis (Vodm) and rostro-dorsomedial areas of the trigeminal subnucleus oralis (Vor) with the ipsilaterally dominant distribution, but hardly in the periaqueductal gray (PAG), dorsal raphe nucleus (DR) and Edinger-Westphal nucleus (EW). Intraperitoneal administration of MK-801 (0.03,0.3 and 3.0 mg/kg) prior to the onset of experimental tooth movement reduced c-Fos in the TSNC (Vc I/II, Vodm and Vor), but increased it in the nucleus raphe magnus (NRM), ventrolateral PAG (vl PAG), DR and EW. These results highly emphasize that during experimental tooth movement, a blockade of NMDA receptors induces neuronal suppression in the TSNC, but increases neuronal activity in the descending antinociceptive system including the NRM, vl PAC, DR and EW.