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Hyperexcitability in Spinal WDR Neurons following Experimental Disc Herniation Is Associated with Upregulation of Fractalkine and Its Receptor in Nucleus Pulposus and the Dorsal Root Ganglion
Introduction. Lumbar radicular pain following intervertebral disc herniation may be associated with a local inflammatory response induced by nucleus pulposus (NP) cells. Methods. In anaesthetized Lewis rats, extracellular single unit recordings of wide dynamic range (WDR) neurons in the dorsal horn...
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Published in: | International Journal of Inflammation 2016-01, Vol.2016 (2016), p.52-61 |
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description | Introduction. Lumbar radicular pain following intervertebral disc herniation may be associated with a local inflammatory response induced by nucleus pulposus (NP) cells. Methods. In anaesthetized Lewis rats, extracellular single unit recordings of wide dynamic range (WDR) neurons in the dorsal horn and qPCR were used to explore the effect of NP application onto the dorsal nerve roots (L3–L5). Results. A clear increase in C-fiber response was observed following NP conditioning. In the NP tissue, the expression of interleukin-1β (IL-1β), colony stimulating factor 1 (Csf1), fractalkine (CX3CL1), and the fractalkine receptor CX3CR1 was increased. Minocycline, an inhibitor of microglial activation, inhibited the increase in neuronal activity and attenuated the increase in IL-1β, Csf1, CX3L1, and CX3CR1 expression in NP tissue. In addition, the results demonstrated an increase in the expression of TNF, CX3CL1, and CX3CR1 in the dorsal root ganglions (DRGs). Conclusion. Hyperexcitability in the pain pathways and the local inflammation after disc herniation may involve upregulation of CX3CL1 signaling in both the NP and the DRG. |
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Lumbar radicular pain following intervertebral disc herniation may be associated with a local inflammatory response induced by nucleus pulposus (NP) cells. Methods. In anaesthetized Lewis rats, extracellular single unit recordings of wide dynamic range (WDR) neurons in the dorsal horn and qPCR were used to explore the effect of NP application onto the dorsal nerve roots (L3–L5). Results. A clear increase in C-fiber response was observed following NP conditioning. In the NP tissue, the expression of interleukin-1β (IL-1β), colony stimulating factor 1 (Csf1), fractalkine (CX3CL1), and the fractalkine receptor CX3CR1 was increased. Minocycline, an inhibitor of microglial activation, inhibited the increase in neuronal activity and attenuated the increase in IL-1β, Csf1, CX3L1, and CX3CR1 expression in NP tissue. In addition, the results demonstrated an increase in the expression of TNF, CX3CL1, and CX3CR1 in the dorsal root ganglions (DRGs). Conclusion. Hyperexcitability in the pain pathways and the local inflammation after disc herniation may involve upregulation of CX3CL1 signaling in both the NP and the DRG.</description><identifier>ISSN: 2042-0099</identifier><identifier>ISSN: 2090-8040</identifier><identifier>EISSN: 2042-0099</identifier><identifier>DOI: 10.1155/2016/6519408</identifier><identifier>PMID: 28116212</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Limiteds</publisher><subject>Animals ; Electrodes ; Experiments ; Gene expression ; Inflammation ; Interleukins ; Kinases ; Neurons ; Software ; Spinal cord ; Tumor necrosis factor-TNF</subject><ispartof>International Journal of Inflammation, 2016-01, Vol.2016 (2016), p.52-61</ispartof><rights>Copyright © 2016 Daniel Pitz Jacobsen et al.</rights><rights>COPYRIGHT 2017 John Wiley & Sons, Inc.</rights><rights>Copyright © 2016 Daniel Pitz Jacobsen et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>info:eu-repo/semantics/openAccess</rights><rights>Copyright © 2016 Daniel Pitz Jacobsen et al. 2016</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-a727t-556f8a5232942cfd08a9b3145d035e8f7366c80354e9869fe0d0632af938da4b3</citedby><cites>FETCH-LOGICAL-a727t-556f8a5232942cfd08a9b3145d035e8f7366c80354e9869fe0d0632af938da4b3</cites><orcidid>0000-0003-3229-6830</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2407638097/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2407638097?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,26567,27924,27925,37012,37013,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28116212$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Hart, David A.</contributor><contributor>David A Hart</contributor><creatorcontrib>Gjerstad, Johannes</creatorcontrib><creatorcontrib>Haugen, Fred</creatorcontrib><creatorcontrib>Moen, Aurora</creatorcontrib><creatorcontrib>Jacobsen, Daniel Pitz</creatorcontrib><title>Hyperexcitability in Spinal WDR Neurons following Experimental Disc Herniation Is Associated with Upregulation of Fractalkine and Its Receptor in Nucleus Pulposus and the Dorsal Root Ganglion</title><title>International Journal of Inflammation</title><addtitle>Int J Inflam</addtitle><description>Introduction. Lumbar radicular pain following intervertebral disc herniation may be associated with a local inflammatory response induced by nucleus pulposus (NP) cells. Methods. In anaesthetized Lewis rats, extracellular single unit recordings of wide dynamic range (WDR) neurons in the dorsal horn and qPCR were used to explore the effect of NP application onto the dorsal nerve roots (L3–L5). Results. A clear increase in C-fiber response was observed following NP conditioning. In the NP tissue, the expression of interleukin-1β (IL-1β), colony stimulating factor 1 (Csf1), fractalkine (CX3CL1), and the fractalkine receptor CX3CR1 was increased. Minocycline, an inhibitor of microglial activation, inhibited the increase in neuronal activity and attenuated the increase in IL-1β, Csf1, CX3L1, and CX3CR1 expression in NP tissue. In addition, the results demonstrated an increase in the expression of TNF, CX3CL1, and CX3CR1 in the dorsal root ganglions (DRGs). Conclusion. Hyperexcitability in the pain pathways and the local inflammation after disc herniation may involve upregulation of CX3CL1 signaling in both the NP and the DRG.</description><subject>Animals</subject><subject>Electrodes</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Inflammation</subject><subject>Interleukins</subject><subject>Kinases</subject><subject>Neurons</subject><subject>Software</subject><subject>Spinal cord</subject><subject>Tumor necrosis factor-TNF</subject><issn>2042-0099</issn><issn>2090-8040</issn><issn>2042-0099</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>PIMPY</sourceid><sourceid>3HK</sourceid><sourceid>DOA</sourceid><recordid>eNqNk11vFCEUhidGY03tndeGxMSY6LbADAzcmDT9XNPUptp4SViG2aXOwgqMbX-df80z3e3HNl44TMIBnvMC53CK4g3B24QwtkMx4TucEVlh8ax4RXFFRxhL-fyRvVFspXSJ4Ssl_PJlsUEFIZwS-qr4c3yzsNFeG5f1xHUu3yDn0beF87pDP_bP0antY_AJtaHrwpXzU3RwDR5ubn0GZN8lg45t9E5nFzwaJ7SbUjAwtA26cnmGLhbRTvtuuR5adBi1AdefzlukfYPGOaFza-wihzhsftqbzvYJnfXdIiQwBijPLNoPMcGW5yFkdKT9tAPB18WLVnfJbq36zeLi8OD73vHo5OvReG_3ZKRrWucRY7wVmtGSyoqatsFCy0lJKtbgklnR1iXnRoBdWSm4bC1uMC-pbmUpGl1Nys1ivNRtgr5UC7i_jjcqaKduJ0KcKh2zg5MrNhEtrYid2ImpJGtEa4m0VW0abmgla9D6vNRa9JO5bQxEMupuTXR9xbuZmobfilFIak1AAC0FTHQpO698iFoRLBhVhJSl4IB8WO0Rw6_epqzmkCnbddrb0CdFBCccM0kkoO-eoJehj5D_pGiFa14KfHvoFTXVcEfn2wBHM4Oo2mWsIoJwJoDa_gcFrbFzZ4K3rYP5NYf3jxxmVnd5lkLXD48lrYOf7u4cUoq2vY8XwWqoBTXUglrVAuBvH8f4Hr57-QB8XAIz5xt95f5TzgJjW_1AE8wpG1LyZQloF112DyE8Ax1GKK6h_G41CR26GsO7xPjpABLISfkX2botpg</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Gjerstad, Johannes</creator><creator>Haugen, Fred</creator><creator>Moen, Aurora</creator><creator>Jacobsen, Daniel Pitz</creator><general>Hindawi Limiteds</general><general>Hindawi Publishing Corporation</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>188</scope><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>NAPCQ</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>3HK</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0003-3229-6830</orcidid></search><sort><creationdate>20160101</creationdate><title>Hyperexcitability in Spinal WDR Neurons following Experimental Disc Herniation Is Associated with Upregulation of Fractalkine and Its Receptor in Nucleus Pulposus and the Dorsal Root Ganglion</title><author>Gjerstad, Johannes ; Haugen, Fred ; Moen, Aurora ; Jacobsen, Daniel Pitz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-a727t-556f8a5232942cfd08a9b3145d035e8f7366c80354e9869fe0d0632af938da4b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Electrodes</topic><topic>Experiments</topic><topic>Gene expression</topic><topic>Inflammation</topic><topic>Interleukins</topic><topic>Kinases</topic><topic>Neurons</topic><topic>Software</topic><topic>Spinal cord</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Gjerstad, Johannes</creatorcontrib><creatorcontrib>Haugen, Fred</creatorcontrib><creatorcontrib>Moen, Aurora</creatorcontrib><creatorcontrib>Jacobsen, Daniel Pitz</creatorcontrib><collection>Airiti Library</collection><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access Journals</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Nursing and Allied Health Source</collection><collection>ProQuest_Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>AUTh Library subscriptions: ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Nursing & Allied Health Premium</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>NORA - Norwegian Open Research Archives</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>International Journal of Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Gjerstad, Johannes</au><au>Haugen, Fred</au><au>Moen, Aurora</au><au>Jacobsen, Daniel Pitz</au><au>Hart, David A.</au><au>David A Hart</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperexcitability in Spinal WDR Neurons following Experimental Disc Herniation Is Associated with Upregulation of Fractalkine and Its Receptor in Nucleus Pulposus and the Dorsal Root Ganglion</atitle><jtitle>International Journal of Inflammation</jtitle><addtitle>Int J Inflam</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>2016</volume><issue>2016</issue><spage>52</spage><epage>61</epage><pages>52-61</pages><issn>2042-0099</issn><issn>2090-8040</issn><eissn>2042-0099</eissn><abstract>Introduction. Lumbar radicular pain following intervertebral disc herniation may be associated with a local inflammatory response induced by nucleus pulposus (NP) cells. Methods. In anaesthetized Lewis rats, extracellular single unit recordings of wide dynamic range (WDR) neurons in the dorsal horn and qPCR were used to explore the effect of NP application onto the dorsal nerve roots (L3–L5). Results. A clear increase in C-fiber response was observed following NP conditioning. In the NP tissue, the expression of interleukin-1β (IL-1β), colony stimulating factor 1 (Csf1), fractalkine (CX3CL1), and the fractalkine receptor CX3CR1 was increased. Minocycline, an inhibitor of microglial activation, inhibited the increase in neuronal activity and attenuated the increase in IL-1β, Csf1, CX3L1, and CX3CR1 expression in NP tissue. In addition, the results demonstrated an increase in the expression of TNF, CX3CL1, and CX3CR1 in the dorsal root ganglions (DRGs). Conclusion. Hyperexcitability in the pain pathways and the local inflammation after disc herniation may involve upregulation of CX3CL1 signaling in both the NP and the DRG.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Limiteds</pub><pmid>28116212</pmid><doi>10.1155/2016/6519408</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0003-3229-6830</orcidid><oa>free_for_read</oa></addata></record> |
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subjects | Animals Electrodes Experiments Gene expression Inflammation Interleukins Kinases Neurons Software Spinal cord Tumor necrosis factor-TNF |
title | Hyperexcitability in Spinal WDR Neurons following Experimental Disc Herniation Is Associated with Upregulation of Fractalkine and Its Receptor in Nucleus Pulposus and the Dorsal Root Ganglion |
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