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Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats
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| Zeitschriftentitel: | European Journal of Pain |
|---|---|
| Personen und Körperschaften: | , , , , , |
| In: | European Journal of Pain, 17, 2013, 7, S. 983-994 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Wiley
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| Schlagwörter: |
| author_facet |
Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. |
|---|---|
| author |
Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. |
| spellingShingle |
Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. European Journal of Pain Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats Anesthesiology and Pain Medicine |
| author_sort |
bi, r‐y. |
| spelling |
Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. 1090-3801 1532-2149 Wiley Anesthesiology and Pain Medicine http://dx.doi.org/10.1002/j.1532-2149.2012.00262.x <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Inflammation is a major cause of temporomandibular disorder‐related pain. The <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 sodium channel has a critical function in pain perceptions. However, whether and how <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal ganglion is involved in temporomandibular joint (<jats:styled-content style="fixed-case">TMJ</jats:styled-content>) inflammatory pain remains to be examined.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation was induced by complete <jats:styled-content style="fixed-case">F</jats:styled-content>reund's adjuvant in female rats. The expression of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and other sodium channels was examined using real‐time polymerase chain reaction or <jats:styled-content style="fixed-case">W</jats:styled-content>estern blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer <jats:styled-content style="fixed-case">DiI</jats:styled-content> was used to confirm <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. The functions of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and extracellular signal‐regulated kinase 1/2 (<jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2) phosphorylation were blocked with the microinjection of the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 antibody or <jats:styled-content style="fixed-case">U</jats:styled-content>0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate <jats:styled-content style="fixed-case">TMJ</jats:styled-content> nociceptive responses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation significantly up‐regulated <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> and protein; however, the <jats:styled-content style="fixed-case">mRNA</jats:styled-content> of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.3 was not affected and those of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.8 and <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.9 were only slightly up‐regulated. <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation specifically induced <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. In addition, blocking the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 function significantly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. Moreover, <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation up‐regulated <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation only in the glials; blocking <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation in the glials blocked <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 up‐regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 has an important function in the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>, which is dependent on the communication with the satellite glials.</jats:p></jats:sec> Involvement of trigeminal ganglionic <scp>N</scp>a<sub>v</sub>1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on <scp>ERK</scp>1/2 phosphorylation of glial cells in rats European Journal of Pain |
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10.1002/j.1532-2149.2012.00262.x |
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Wiley, 2013 |
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1090-3801 1532-2149 |
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bi2013involvementoftrigeminalganglionicnav17inhyperalgesiaofinflamedtemporomandibularjointisdependentonerk12phosphorylationofglialcellsinrats |
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2013 |
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European Journal of Pain |
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49 |
| title |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_unstemmed |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_full |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_fullStr |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_full_unstemmed |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_short |
Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_sort |
involvement of trigeminal ganglionic <scp>n</scp>a<sub>v</sub>1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on <scp>erk</scp>1/2 phosphorylation of glial cells in rats |
| topic |
Anesthesiology and Pain Medicine |
| url |
http://dx.doi.org/10.1002/j.1532-2149.2012.00262.x |
| publishDate |
2013 |
| physical |
983-994 |
| description |
<jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Inflammation is a major cause of temporomandibular disorder‐related pain. The <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 sodium channel has a critical function in pain perceptions. However, whether and how <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal ganglion is involved in temporomandibular joint (<jats:styled-content style="fixed-case">TMJ</jats:styled-content>) inflammatory pain remains to be examined.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation was induced by complete <jats:styled-content style="fixed-case">F</jats:styled-content>reund's adjuvant in female rats. The expression of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and other sodium channels was examined using real‐time polymerase chain reaction or <jats:styled-content style="fixed-case">W</jats:styled-content>estern blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer <jats:styled-content style="fixed-case">DiI</jats:styled-content> was used to confirm <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. The functions of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and extracellular signal‐regulated kinase 1/2 (<jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2) phosphorylation were blocked with the microinjection of the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 antibody or <jats:styled-content style="fixed-case">U</jats:styled-content>0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate <jats:styled-content style="fixed-case">TMJ</jats:styled-content> nociceptive responses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation significantly up‐regulated <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> and protein; however, the <jats:styled-content style="fixed-case">mRNA</jats:styled-content> of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.3 was not affected and those of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.8 and <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.9 were only slightly up‐regulated. <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation specifically induced <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. In addition, blocking the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 function significantly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. Moreover, <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation up‐regulated <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation only in the glials; blocking <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation in the glials blocked <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 up‐regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 has an important function in the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>, which is dependent on the communication with the satellite glials.</jats:p></jats:sec> |
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| author | Bi, R‐Y., Kou, X‐X., Meng, Z., Wang, X‐D., Ding, Y., Gan, Y‐H. |
| author_facet | Bi, R‐Y., Kou, X‐X., Meng, Z., Wang, X‐D., Ding, Y., Gan, Y‐H., Bi, R‐Y., Kou, X‐X., Meng, Z., Wang, X‐D., Ding, Y., Gan, Y‐H. |
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| container_start_page | 983 |
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| description | <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Inflammation is a major cause of temporomandibular disorder‐related pain. The <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 sodium channel has a critical function in pain perceptions. However, whether and how <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal ganglion is involved in temporomandibular joint (<jats:styled-content style="fixed-case">TMJ</jats:styled-content>) inflammatory pain remains to be examined.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation was induced by complete <jats:styled-content style="fixed-case">F</jats:styled-content>reund's adjuvant in female rats. The expression of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and other sodium channels was examined using real‐time polymerase chain reaction or <jats:styled-content style="fixed-case">W</jats:styled-content>estern blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer <jats:styled-content style="fixed-case">DiI</jats:styled-content> was used to confirm <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. The functions of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and extracellular signal‐regulated kinase 1/2 (<jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2) phosphorylation were blocked with the microinjection of the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 antibody or <jats:styled-content style="fixed-case">U</jats:styled-content>0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate <jats:styled-content style="fixed-case">TMJ</jats:styled-content> nociceptive responses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation significantly up‐regulated <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> and protein; however, the <jats:styled-content style="fixed-case">mRNA</jats:styled-content> of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.3 was not affected and those of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.8 and <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.9 were only slightly up‐regulated. <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation specifically induced <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. In addition, blocking the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 function significantly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. Moreover, <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation up‐regulated <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation only in the glials; blocking <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation in the glials blocked <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 up‐regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 has an important function in the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>, which is dependent on the communication with the satellite glials.</jats:p></jats:sec> |
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| series | European Journal of Pain |
| source_id | 49 |
| spelling | Bi, R‐Y. Kou, X‐X. Meng, Z. Wang, X‐D. Ding, Y. Gan, Y‐H. 1090-3801 1532-2149 Wiley Anesthesiology and Pain Medicine http://dx.doi.org/10.1002/j.1532-2149.2012.00262.x <jats:title>Abstract</jats:title><jats:sec><jats:title>Background</jats:title><jats:p>Inflammation is a major cause of temporomandibular disorder‐related pain. The <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 sodium channel has a critical function in pain perceptions. However, whether and how <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal ganglion is involved in temporomandibular joint (<jats:styled-content style="fixed-case">TMJ</jats:styled-content>) inflammatory pain remains to be examined.</jats:p></jats:sec><jats:sec><jats:title>Methods</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation was induced by complete <jats:styled-content style="fixed-case">F</jats:styled-content>reund's adjuvant in female rats. The expression of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and other sodium channels was examined using real‐time polymerase chain reaction or <jats:styled-content style="fixed-case">W</jats:styled-content>estern blotting. Immunohistofluorescence with fluorescent retrograde neuronal tracer <jats:styled-content style="fixed-case">DiI</jats:styled-content> was used to confirm <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the trigeminal neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. The functions of trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 and extracellular signal‐regulated kinase 1/2 (<jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2) phosphorylation were blocked with the microinjection of the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 antibody or <jats:styled-content style="fixed-case">U</jats:styled-content>0126 into the trigeminal ganglion. Head withdrawal threshold and food intake was measured to evaluate <jats:styled-content style="fixed-case">TMJ</jats:styled-content> nociceptive responses.</jats:p></jats:sec><jats:sec><jats:title>Results</jats:title><jats:p><jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation significantly up‐regulated <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 <jats:styled-content style="fixed-case">mRNA</jats:styled-content> and protein; however, the <jats:styled-content style="fixed-case">mRNA</jats:styled-content> of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.3 was not affected and those of <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.8 and <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.9 were only slightly up‐regulated. <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation specifically induced <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 in the neurons innervating <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. In addition, blocking the <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 function significantly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>. Moreover, <jats:styled-content style="fixed-case">TMJ</jats:styled-content> inflammation up‐regulated <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation only in the glials; blocking <jats:styled-content style="fixed-case">ERK</jats:styled-content>1/2 phosphorylation in the glials blocked <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 up‐regulation in the neurons and correspondingly attenuated the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>.</jats:p></jats:sec><jats:sec><jats:title>Conclusions</jats:title><jats:p>Trigeminal ganglionic <jats:styled-content style="fixed-case">N</jats:styled-content>a<jats:sub>v</jats:sub>1.7 has an important function in the hyperalgesia of the inflamed <jats:styled-content style="fixed-case">TMJ</jats:styled-content>, which is dependent on the communication with the satellite glials.</jats:p></jats:sec> Involvement of trigeminal ganglionic <scp>N</scp>a<sub>v</sub>1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on <scp>ERK</scp>1/2 phosphorylation of glial cells in rats European Journal of Pain |
| spellingShingle | Bi, R‐Y., Kou, X‐X., Meng, Z., Wang, X‐D., Ding, Y., Gan, Y‐H., European Journal of Pain, Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats, Anesthesiology and Pain Medicine |
| title | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_full | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_fullStr | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_full_unstemmed | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_short | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| title_sort | involvement of trigeminal ganglionic <scp>n</scp>a<sub>v</sub>1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on <scp>erk</scp>1/2 phosphorylation of glial cells in rats |
| title_unstemmed | Involvement of trigeminal ganglionic Nav1.7 in hyperalgesia of inflamed temporomandibular joint is dependent on ERK1/2 phosphorylation of glial cells in rats |
| topic | Anesthesiology and Pain Medicine |
| url | http://dx.doi.org/10.1002/j.1532-2149.2012.00262.x |