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Involvement of trigeminal ganglionic Nav 1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats.
Eur J Pain. 2013 Aug; 17(7):983-94.EJ

Abstract

BACKGROUND

Inflammation is a major cause of temporomandibular disorder-related pain. The Nav 1.7 sodium channel has a critical function in pain perceptions. However, whether and how Nav 1.7 in the trigeminal ganglion is involved in temporomandibular joint (TMJ) inflammatory pain remains to be examined.

METHODS

TMJ inflammation was induced by complete Freund's adjuvant in female rats. The expression of trigeminal ganglionic Nav 1.7 and other sodium channels was examined using real-time polymerase chain reaction or Western blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer DiI was used to confirm Nav 1.7 in the trigeminal neurons innervating TMJ. The functions of trigeminal ganglionic Nav 1.7 and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation were blocked with the microinjection of the Nav 1.7 antibody or U0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate TMJ nociceptive responses.

RESULTS

TMJ inflammation significantly up-regulated Nav 1.7 mRNA and protein; however, the mRNA of Nav 1.3 was not affected and those of Nav 1.8 and Nav 1.9 were only slightly up-regulated. TMJ inflammation specifically induced Nav 1.7 in the neurons innervating TMJ. In addition, blocking the Nav 1.7 function significantly attenuated the hyperalgesia of the inflamed TMJ. Moreover, TMJ inflammation up-regulated ERK1/2 phosphorylation only in the glials; blocking ERK1/2 phosphorylation in the glials blocked Nav 1.7 up-regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed TMJ.

CONCLUSIONS

Trigeminal ganglionic Nav 1.7 has an important function in the hyperalgesia of the inflamed TMJ, which is dependent on the communication with the satellite glials.

Authors+Show Affiliations

The Third Dental Center, Peking University School and Hospital of Stomatology, Beijing, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

23242737

Citation

Bi, R-Y, et al. "Involvement of Trigeminal Ganglionic Nav 1.7 in Hyperalgesia of Inflamed Temporomandibular Joint Is Dependent On ERK1/2 Phosphorylation of Glial Cells in Rats." European Journal of Pain (London, England), vol. 17, no. 7, 2013, pp. 983-94.
Bi RY, Kou XX, Meng Z, et al. Involvement of trigeminal ganglionic Nav 1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats. Eur J Pain. 2013;17(7):983-94.
Bi, R. Y., Kou, X. X., Meng, Z., Wang, X. D., Ding, Y., & Gan, Y. H. (2013). Involvement of trigeminal ganglionic Nav 1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats. European Journal of Pain (London, England), 17(7), 983-94. https://doi.org/10.1002/j.1532-2149.2012.00262.x
Bi RY, et al. Involvement of Trigeminal Ganglionic Nav 1.7 in Hyperalgesia of Inflamed Temporomandibular Joint Is Dependent On ERK1/2 Phosphorylation of Glial Cells in Rats. Eur J Pain. 2013;17(7):983-94. PubMed PMID: 23242737.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Involvement of trigeminal ganglionic Nav 1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats. AU - Bi,R-Y, AU - Kou,X-X, AU - Meng,Z, AU - Wang,X-D, AU - Ding,Y, AU - Gan,Y-H, Y1 - 2012/12/14/ PY - 2012/11/14/accepted PY - 2012/12/18/entrez PY - 2012/12/18/pubmed PY - 2014/3/22/medline SP - 983 EP - 94 JF - European journal of pain (London, England) JO - Eur J Pain VL - 17 IS - 7 N2 - BACKGROUND: Inflammation is a major cause of temporomandibular disorder-related pain. The Nav 1.7 sodium channel has a critical function in pain perceptions. However, whether and how Nav 1.7 in the trigeminal ganglion is involved in temporomandibular joint (TMJ) inflammatory pain remains to be examined. METHODS: TMJ inflammation was induced by complete Freund's adjuvant in female rats. The expression of trigeminal ganglionic Nav 1.7 and other sodium channels was examined using real-time polymerase chain reaction or Western blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer DiI was used to confirm Nav 1.7 in the trigeminal neurons innervating TMJ. The functions of trigeminal ganglionic Nav 1.7 and extracellular signal-regulated kinase 1/2 (ERK1/2) phosphorylation were blocked with the microinjection of the Nav 1.7 antibody or U0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate TMJ nociceptive responses. RESULTS: TMJ inflammation significantly up-regulated Nav 1.7 mRNA and protein; however, the mRNA of Nav 1.3 was not affected and those of Nav 1.8 and Nav 1.9 were only slightly up-regulated. TMJ inflammation specifically induced Nav 1.7 in the neurons innervating TMJ. In addition, blocking the Nav 1.7 function significantly attenuated the hyperalgesia of the inflamed TMJ. Moreover, TMJ inflammation up-regulated ERK1/2 phosphorylation only in the glials; blocking ERK1/2 phosphorylation in the glials blocked Nav 1.7 up-regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed TMJ. CONCLUSIONS: Trigeminal ganglionic Nav 1.7 has an important function in the hyperalgesia of the inflamed TMJ, which is dependent on the communication with the satellite glials. SN - 1532-2149 UR - https://www.unboundmedicine.com/medline/citation/23242737/Involvement_of_trigeminal_ganglionic_Nav_1_7_in_hyperalgesia_of_inflamed_temporomandibular_joint_is_dependent_on_ERK1/2_phosphorylation_of_glial_cells_in_rats_ L2 - https://doi.org/10.1002/j.1532-2149.2012.00262.x DB - PRIME DP - Unbound Medicine ER -