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PKCγ in Vc and C1/C2 is Involved in Trigeminal Neuropathic Pain
The aim of the present study was to clarify the involvement of protein kinase Cγ (PKCγ) in the facial neuropathic pain following infraorbital nerve injury. We analyzed the change in PKCγ expression in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1/C2) following chr...
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Published in: | Journal of dental research 2011-06, Vol.90 (6), p.777-781 |
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creator | Nakajima, A. Tsuboi, Y. Suzuki, I. Honda, K. Shinoda, M. Kondo, M. Matsuura, S. Shibuta, K. Yasuda, M. Shimizu, N. Iwata, K. |
description | The aim of the present study was to clarify the involvement of protein kinase Cγ (PKCγ) in the facial neuropathic pain following infraorbital nerve injury. We analyzed the change in PKCγ expression in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1/C2) following chronic constriction injury of the infraorbital nerve (ION-CCI). We also studied ION-CCI-mediated mechanical nocifensive behavior in rats. The mechanical head-withdrawal threshold significantly decreased 1 to 14 days after ION-CCI compared with that before ION-CCI and in sham rats. The expression of PKCγ was significantly larger in the ipsilateral Vc compared with the contralateral side in ION-CCI rats 3, 7, and 14 days after ION-CCI. Intrathecal (i.t.) administration of the PKCγ inhibitor chelerythrine prevented an increase in the PKCγ expression in the ipsilateral Vc. Moreover, i.t. administration of chelerythrine annulled ION-CCI-mediated reduction in the head-withdrawal threshold. Taken together, these findings suggest that PKCγ expression in the Vc played an important role in the mechanism of orofacial static mechanical allodynia following trigeminal nerve injury. |
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We analyzed the change in PKCγ expression in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1/C2) following chronic constriction injury of the infraorbital nerve (ION-CCI). We also studied ION-CCI-mediated mechanical nocifensive behavior in rats. The mechanical head-withdrawal threshold significantly decreased 1 to 14 days after ION-CCI compared with that before ION-CCI and in sham rats. The expression of PKCγ was significantly larger in the ipsilateral Vc compared with the contralateral side in ION-CCI rats 3, 7, and 14 days after ION-CCI. Intrathecal (i.t.) administration of the PKCγ inhibitor chelerythrine prevented an increase in the PKCγ expression in the ipsilateral Vc. Moreover, i.t. administration of chelerythrine annulled ION-CCI-mediated reduction in the head-withdrawal threshold. Taken together, these findings suggest that PKCγ expression in the Vc played an important role in the mechanism of orofacial static mechanical allodynia following trigeminal nerve injury.</description><identifier>ISSN: 0022-0345</identifier><identifier>EISSN: 1544-0591</identifier><identifier>DOI: 10.1177/0022034511401406</identifier><language>eng</language><publisher>Los Angeles, CA: SAGE Publications</publisher><subject>Biological and medical sciences ; Chelerythrine ; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction ; Kinases ; Mechanical properties ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neuralgia ; Neurology ; Pain perception ; Protein kinase ; Protein kinase C ; Spinal cord injuries ; Trigeminal nerve</subject><ispartof>Journal of dental research, 2011-06, Vol.90 (6), p.777-781</ispartof><rights>2011 International & American Associations for Dental Research</rights><rights>2015 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c368t-57359d71995a5e95562b03b277ae75950ab5c8c52ab4919d81229c431a862cab3</citedby><cites>FETCH-LOGICAL-c368t-57359d71995a5e95562b03b277ae75950ab5c8c52ab4919d81229c431a862cab3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,786,790,27957,27958</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24249020$$DView record in Pascal Francis$$Hfree_for_read</backlink></links><search><creatorcontrib>Nakajima, A.</creatorcontrib><creatorcontrib>Tsuboi, Y.</creatorcontrib><creatorcontrib>Suzuki, I.</creatorcontrib><creatorcontrib>Honda, K.</creatorcontrib><creatorcontrib>Shinoda, M.</creatorcontrib><creatorcontrib>Kondo, M.</creatorcontrib><creatorcontrib>Matsuura, S.</creatorcontrib><creatorcontrib>Shibuta, K.</creatorcontrib><creatorcontrib>Yasuda, M.</creatorcontrib><creatorcontrib>Shimizu, N.</creatorcontrib><creatorcontrib>Iwata, K.</creatorcontrib><title>PKCγ in Vc and C1/C2 is Involved in Trigeminal Neuropathic Pain</title><title>Journal of dental research</title><description>The aim of the present study was to clarify the involvement of protein kinase Cγ (PKCγ) in the facial neuropathic pain following infraorbital nerve injury. We analyzed the change in PKCγ expression in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1/C2) following chronic constriction injury of the infraorbital nerve (ION-CCI). We also studied ION-CCI-mediated mechanical nocifensive behavior in rats. The mechanical head-withdrawal threshold significantly decreased 1 to 14 days after ION-CCI compared with that before ION-CCI and in sham rats. The expression of PKCγ was significantly larger in the ipsilateral Vc compared with the contralateral side in ION-CCI rats 3, 7, and 14 days after ION-CCI. Intrathecal (i.t.) administration of the PKCγ inhibitor chelerythrine prevented an increase in the PKCγ expression in the ipsilateral Vc. Moreover, i.t. administration of chelerythrine annulled ION-CCI-mediated reduction in the head-withdrawal threshold. Taken together, these findings suggest that PKCγ expression in the Vc played an important role in the mechanism of orofacial static mechanical allodynia following trigeminal nerve injury.</description><subject>Biological and medical sciences</subject><subject>Chelerythrine</subject><subject>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</subject><subject>Kinases</subject><subject>Mechanical properties</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neuralgia</subject><subject>Neurology</subject><subject>Pain perception</subject><subject>Protein kinase</subject><subject>Protein kinase C</subject><subject>Spinal cord injuries</subject><subject>Trigeminal nerve</subject><issn>0022-0345</issn><issn>1544-0591</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><recordid>eNp1kMtKw0AUhgdRsFb3LgfEZeyZW5LZKcFLsWgX1W04mUzrlDSpM03B5_I9fCYTWhQE4cBZ_P__nQsh5wyuGEuSEQDnIKRiTEJX8QEZMCVlBEqzQzLo5ajXj8lJCEsApnkqBuR6-ph9fVJX01dDsS5pxkYZpy7Qcb1tqq0te23m3cKuXI0VfbKtb9a4eXOGTtHVp-RojlWwZ_s-JC93t7PsIZo834-zm0lkRJxuIpUIpcuEaa1QWa1UzAsQBU8StInSCrBQJjWKYyE102XKONdGCoZpzA0WYkgudty1b95bGzb5sml9t1HIuQCIWXc6dC7YuYxvQvB2nq-9W6H_yBnk_Z_yv3_qIpd7MAaD1dxjbVz4yXHJpQbeo6OdL-DC_g7_l_sNx51wOQ</recordid><startdate>20110601</startdate><enddate>20110601</enddate><creator>Nakajima, A.</creator><creator>Tsuboi, Y.</creator><creator>Suzuki, I.</creator><creator>Honda, K.</creator><creator>Shinoda, M.</creator><creator>Kondo, M.</creator><creator>Matsuura, S.</creator><creator>Shibuta, K.</creator><creator>Yasuda, M.</creator><creator>Shimizu, N.</creator><creator>Iwata, K.</creator><general>SAGE Publications</general><general>International Association for Dental Research</general><general>SAGE PUBLICATIONS, INC</general><scope>IQODW</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope></search><sort><creationdate>20110601</creationdate><title>PKCγ in Vc and C1/C2 is Involved in Trigeminal Neuropathic Pain</title><author>Nakajima, A. ; Tsuboi, Y. ; Suzuki, I. ; Honda, K. ; Shinoda, M. ; Kondo, M. ; Matsuura, S. ; Shibuta, K. ; Yasuda, M. ; Shimizu, N. ; Iwata, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c368t-57359d71995a5e95562b03b277ae75950ab5c8c52ab4919d81229c431a862cab3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Biological and medical sciences</topic><topic>Chelerythrine</topic><topic>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>Kinases</topic><topic>Mechanical properties</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neuralgia</topic><topic>Neurology</topic><topic>Pain perception</topic><topic>Protein kinase</topic><topic>Protein kinase C</topic><topic>Spinal cord injuries</topic><topic>Trigeminal nerve</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nakajima, A.</creatorcontrib><creatorcontrib>Tsuboi, Y.</creatorcontrib><creatorcontrib>Suzuki, I.</creatorcontrib><creatorcontrib>Honda, K.</creatorcontrib><creatorcontrib>Shinoda, M.</creatorcontrib><creatorcontrib>Kondo, M.</creatorcontrib><creatorcontrib>Matsuura, S.</creatorcontrib><creatorcontrib>Shibuta, K.</creatorcontrib><creatorcontrib>Yasuda, M.</creatorcontrib><creatorcontrib>Shimizu, N.</creatorcontrib><creatorcontrib>Iwata, K.</creatorcontrib><collection>Pascal-Francis</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>Journal of dental research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nakajima, A.</au><au>Tsuboi, Y.</au><au>Suzuki, I.</au><au>Honda, K.</au><au>Shinoda, M.</au><au>Kondo, M.</au><au>Matsuura, S.</au><au>Shibuta, K.</au><au>Yasuda, M.</au><au>Shimizu, N.</au><au>Iwata, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>PKCγ in Vc and C1/C2 is Involved in Trigeminal Neuropathic Pain</atitle><jtitle>Journal of dental research</jtitle><date>2011-06-01</date><risdate>2011</risdate><volume>90</volume><issue>6</issue><spage>777</spage><epage>781</epage><pages>777-781</pages><issn>0022-0345</issn><eissn>1544-0591</eissn><abstract>The aim of the present study was to clarify the involvement of protein kinase Cγ (PKCγ) in the facial neuropathic pain following infraorbital nerve injury. We analyzed the change in PKCγ expression in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1/C2) following chronic constriction injury of the infraorbital nerve (ION-CCI). We also studied ION-CCI-mediated mechanical nocifensive behavior in rats. The mechanical head-withdrawal threshold significantly decreased 1 to 14 days after ION-CCI compared with that before ION-CCI and in sham rats. The expression of PKCγ was significantly larger in the ipsilateral Vc compared with the contralateral side in ION-CCI rats 3, 7, and 14 days after ION-CCI. Intrathecal (i.t.) administration of the PKCγ inhibitor chelerythrine prevented an increase in the PKCγ expression in the ipsilateral Vc. Moreover, i.t. administration of chelerythrine annulled ION-CCI-mediated reduction in the head-withdrawal threshold. Taken together, these findings suggest that PKCγ expression in the Vc played an important role in the mechanism of orofacial static mechanical allodynia following trigeminal nerve injury.</abstract><cop>Los Angeles, CA</cop><pub>SAGE Publications</pub><doi>10.1177/0022034511401406</doi><tpages>5</tpages></addata></record> |
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subjects | Biological and medical sciences Chelerythrine Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction Kinases Mechanical properties Medical sciences Nervous system (semeiology, syndromes) Neuralgia Neurology Pain perception Protein kinase Protein kinase C Spinal cord injuries Trigeminal nerve |
title | PKCγ in Vc and C1/C2 is Involved in Trigeminal Neuropathic Pain |
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