Administration of MK-801 decreases c-Fos expression in the trigeminal sensory nuclear complex but increases it in the midbrain during experimental movement of rat molars.
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 noncompetitive 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 midbrain 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 PAG, DR and EW.
Hattori
Yukiko
Y
Department of Orthodontics and Craniofacial Developmental Biology, Hiroshima University Graduate School of Biomedical Sciences, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8553, Japan. yhatto@hiroshima-u.ac.jp
Watanabe
Mineo
M
Iwabe
Tatsunori
T
Tanaka
Eiji
E
Nishi
Mika
M
Aoyama
Junko
J
Satoda
Takahiro
T
Uchida
Takashi
T
Tanne
Kazuo
K
D000818:Animals; D001921:Brain / Q000187:drug effects / Q000378:metabolism; D016291:Dizocilpine Maleate / Q000494:pharmacology*; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology*; D007150:Immunohistochemistry; D008297:Male; D008636:Mesencephalon / Q000187:drug effects / Q000378:metabolism*; D008963:Molar / Q000503:physiopathology; D009474:Neurons / Q000187:drug effects / Q000378:metabolism; D010146:Pain / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis* / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D014085:Tooth Migration / Q000503:physiopathology; D014278:Trigeminal Nuclei / Q000187:drug effects / Q000378:metabolism*
D018691:Excitatory Amino Acid Antagonists; D016760:Proto-Oncogene Proteins c-fos; D016291:Dizocilpine Maleate