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Role of NMDA receptors in the trigeminal pathway, and the modulatory effect of magnesium in a model of rat temporomandibular joint arthritis
Author(s) -
Cavalcante André L. C.,
Siqueira Rafaelly M. P.,
Araujo Joana C. B.,
Gondim Delane V.,
Ribeiro Ronaldo A.,
Quetz Josiane S.,
Havt Alexandre,
Lima Aldo A. M.,
Vale Mariana L.
Publication year - 2013
Publication title -
european journal of oral sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.802
H-Index - 93
eISSN - 1600-0722
pISSN - 0909-8836
DOI - 10.1111/eos.12093
Subject(s) - nociception , nmda receptor , temporomandibular joint , immunostaining , medicine , endocrinology , arthritis , chemistry , magnesium deficiency (plants) , magnesium , antagonist , anesthesia , receptor , pharmacology , immunohistochemistry , pathology , organic chemistry
Temporomandibular joint ( TMJ ) arthritis is a common cause of orofacial pain. In the present study, the modulatory effects of N ‐methyl‐ d ‐aspartate receptors ( NMDA ‐ R s) and magnesium were investigated in TMJ arthritis hypernociception. Male Wistar rats received an intra‐articular injection of carrageenan ( C g) in the TMJ , and mechanical hypernociception was measured. The NMDA‐R antagonist, MK ‐801, and magnesium chloride ( M g C l 2 ) were administered before arthritis induction. Magnesium deficiency was promoted by feeding rats a synthetic magnesium‐free diet for 9 d before injection of C g. The C g induced mechanical hypernociception that lasted for 120 h. MK‐801 inhibited this hypernociceptive state. MgCl 2 pretreatment prevented C g‐induced hypernociception and altered the nociceptive threshold in the absence of C g. Magnesium deficiency increased hypernociception and induced spontaneous hypernociceptive behavior. TMJ arthritis increased the expression of mRNA for all NMDA‐R subunits and immunostaining of phosphorylated NR 1 (phospho‐ NR 1). MgCl 2 inhibited expression of NR 2 B mRNA and phospho‐NR1 immunostaining and increased expression of NR3 mRNA . Magnesium deficiency increased expression of both NR 1 and NR 3 mRNA s and phospho‐ NR 1 immunostaining in the trigeminal subnucleus caudalis. We found that magnesium modulates nociceptive behavior and induces NMDA‐R subunit rearrangement in the subnucleus caudalis. The present results may lead to a better understanding of central processing in the nociceptive trigeminal pathway and the development of new approaches to treat orofacial pain with a TMJ origin.

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