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Peripheral N-methyl-d-aspartate receptors contribute to mechanical hypersensitivity in a rat model of inflammatory temporomandibular joint pain.
Eur J Pain. 2011 Feb; 15(2):179-85.EJ

Abstract

The aim of this study was to determine whether peripheral N-methyl-d-aspartate (NMDA) receptors are involved in inflammation-induced mechanical hypersensitivity of the temporomandibular joint (TMJ) region. We developed a rat model of mechanical sensitivity to Complete Freund's Adjuvant (CFA; 2μl containing 1μg Mycobacterium tuberculosis)-induced inflammation of the TMJ and examined changes in sensitivity following injection of NMDA receptor antagonists (dl-2-amino-5-phosphonovaleric acid (AP5) or Ifenprodil) with CFA. CFA injected into the TMJ resulted in an increase in mechanical sensitivity relative to pre-injection that peaked at day 1 and lasted for up to 3days (n=8, P<0.05). There was no change in mechanical sensitivity in vehicle-injected rats at any time-point (n=9). At day 1, there was a significant increase in mechanical sensitivity in animals injected with CFA+vehicle (n=7) relative to those injected with vehicle alone (n=7, P<0.05), and co-injection of AP5 (n=6) or Ifenprodil (n=7) with CFA blocked this hypersensitivity. Subcutaneous injection of AP5 (n=7) and Ifenprodil (n=5) instead of into the TMJ had no significant effect on CFA-induced hypersensitivity of the TMJ region. Western blot analysis revealed constitutive expression of the NR1 and NR2B subunits in trigeminal ganglion lysates. Immunohistochemical studies showed that 99% and 28% of trigeminal ganglion neurons that innervated the TMJ contained the NR1 and NR2B subunits respectively. Our findings suggest a role for peripheral NMDA receptors in inflammation-induced pain of the TMJ region. Targeting peripheral NMDA receptors with peripheral application of NMDA receptor antagonists could provide therapeutic benefit and avoid side effects associated with blockade of NMDA receptors in the central nervous system.

Authors+Show Affiliations

Department of Anatomy and Cell Biology, University of Melbourne, Melbourne 3010, Australia.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20675160

Citation

Ivanusic, J J., et al. "Peripheral N-methyl-d-aspartate Receptors Contribute to Mechanical Hypersensitivity in a Rat Model of Inflammatory Temporomandibular Joint Pain." European Journal of Pain (London, England), vol. 15, no. 2, 2011, pp. 179-85.
Ivanusic JJ, Beaini D, Hatch RJ, et al. Peripheral N-methyl-d-aspartate receptors contribute to mechanical hypersensitivity in a rat model of inflammatory temporomandibular joint pain. Eur J Pain. 2011;15(2):179-85.
Ivanusic, J. J., Beaini, D., Hatch, R. J., Staikopoulos, V., Sessle, B. J., & Jennings, E. A. (2011). Peripheral N-methyl-d-aspartate receptors contribute to mechanical hypersensitivity in a rat model of inflammatory temporomandibular joint pain. European Journal of Pain (London, England), 15(2), 179-85. https://doi.org/10.1016/j.ejpain.2010.07.001
Ivanusic JJ, et al. Peripheral N-methyl-d-aspartate Receptors Contribute to Mechanical Hypersensitivity in a Rat Model of Inflammatory Temporomandibular Joint Pain. Eur J Pain. 2011;15(2):179-85. PubMed PMID: 20675160.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Peripheral N-methyl-d-aspartate receptors contribute to mechanical hypersensitivity in a rat model of inflammatory temporomandibular joint pain. AU - Ivanusic,J J, AU - Beaini,D, AU - Hatch,R J, AU - Staikopoulos,V, AU - Sessle,B J, AU - Jennings,E A, Y1 - 2010/08/02/ PY - 2010/03/05/received PY - 2010/07/07/revised PY - 2010/07/07/accepted PY - 2010/8/3/entrez PY - 2010/8/3/pubmed PY - 2011/5/7/medline SP - 179 EP - 85 JF - European journal of pain (London, England) JO - Eur J Pain VL - 15 IS - 2 N2 - The aim of this study was to determine whether peripheral N-methyl-d-aspartate (NMDA) receptors are involved in inflammation-induced mechanical hypersensitivity of the temporomandibular joint (TMJ) region. We developed a rat model of mechanical sensitivity to Complete Freund's Adjuvant (CFA; 2μl containing 1μg Mycobacterium tuberculosis)-induced inflammation of the TMJ and examined changes in sensitivity following injection of NMDA receptor antagonists (dl-2-amino-5-phosphonovaleric acid (AP5) or Ifenprodil) with CFA. CFA injected into the TMJ resulted in an increase in mechanical sensitivity relative to pre-injection that peaked at day 1 and lasted for up to 3days (n=8, P<0.05). There was no change in mechanical sensitivity in vehicle-injected rats at any time-point (n=9). At day 1, there was a significant increase in mechanical sensitivity in animals injected with CFA+vehicle (n=7) relative to those injected with vehicle alone (n=7, P<0.05), and co-injection of AP5 (n=6) or Ifenprodil (n=7) with CFA blocked this hypersensitivity. Subcutaneous injection of AP5 (n=7) and Ifenprodil (n=5) instead of into the TMJ had no significant effect on CFA-induced hypersensitivity of the TMJ region. Western blot analysis revealed constitutive expression of the NR1 and NR2B subunits in trigeminal ganglion lysates. Immunohistochemical studies showed that 99% and 28% of trigeminal ganglion neurons that innervated the TMJ contained the NR1 and NR2B subunits respectively. Our findings suggest a role for peripheral NMDA receptors in inflammation-induced pain of the TMJ region. Targeting peripheral NMDA receptors with peripheral application of NMDA receptor antagonists could provide therapeutic benefit and avoid side effects associated with blockade of NMDA receptors in the central nervous system. SN - 1532-2149 UR - https://www.unboundmedicine.com/medline/citation/20675160/Peripheral_N_methyl_d_aspartate_receptors_contribute_to_mechanical_hypersensitivity_in_a_rat_model_of_inflammatory_temporomandibular_joint_pain_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S1090-3801(10)00167-9 DB - PRIME DP - Unbound Medicine ER -