Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord
The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABA...
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| Veröffentlicht in: | Pain (Amsterdam) 2009-06, Vol.143 (3), p.228-232 |
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| creator | Tambeli, Claudia H. Levine, Jon D. Gear, Robert W. |
| description | The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors. |
| doi_str_mv | 10.1016/j.pain.2009.03.005 |
| format | Article |
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We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors.</description><identifier>ISSN: 0304-3959</identifier><identifier>EISSN: 1872-6623</identifier><identifier>DOI: 10.1016/j.pain.2009.03.005</identifier><identifier>PMID: 19375225</identifier><identifier>CODEN: PAINDB</identifier><language>eng</language><publisher>Philadelphia, PA: Elsevier B.V</publisher><subject>Analgesics - antagonists & inhibitors ; Animals ; Antinociception ; Baclofen - pharmacology ; Biological and medical sciences ; Capsaicin ; Capsaicin - antagonists & inhibitors ; Drug Interactions - physiology ; Fundamental and applied biological sciences. Psychology ; GABA Agonists - pharmacology ; GABA Antagonists - pharmacology ; GABA-B Receptor Agonists ; GABA-B Receptor Antagonists ; Injuries of the nervous system and the skull. Diseases due to physical agents ; Male ; Medical sciences ; Narcotic Antagonists - pharmacology ; Neural Inhibition - drug effects ; Neural Inhibition - physiology ; Nucleus accumbens ; Pain - chemically induced ; Pain - physiopathology ; Pain Threshold - drug effects ; Pain Threshold - physiology ; Pain-induced analgesia ; Peptides - pharmacology ; Rat ; Rats ; Rats, Sprague-Dawley ; Receptors, GABA-B - metabolism ; Receptors, Opioid, mu - antagonists & inhibitors ; Receptors, Opioid, mu - metabolism ; Sensory System Agents - antagonists & inhibitors ; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors ; Spinal cord ; Spinal Cord - drug effects ; Spinal Cord - physiology ; Synapses - drug effects ; Synapses - physiology ; Synaptic Transmission - drug effects ; Synaptic Transmission - physiology ; Traumas. Diseases due to physical agents ; Vertebrates: nervous system and sense organs</subject><ispartof>Pain (Amsterdam), 2009-06, Vol.143 (3), p.228-232</ispartof><rights>2009 International Association for the Study of Pain</rights><rights>Lippincott Williams & Wilkins, Inc.</rights><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5944-153e9c04662019304816bd563ad40bd63cc8c300b01e209ff34487de7d90111b3</citedby><cites>FETCH-LOGICAL-c5944-153e9c04662019304816bd563ad40bd63cc8c300b01e209ff34487de7d90111b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21534512$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19375225$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Tambeli, Claudia H.</creatorcontrib><creatorcontrib>Levine, Jon D.</creatorcontrib><creatorcontrib>Gear, Robert W.</creatorcontrib><title>Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord</title><title>Pain (Amsterdam)</title><addtitle>Pain</addtitle><description>The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors.</description><subject>Analgesics - antagonists & inhibitors</subject><subject>Animals</subject><subject>Antinociception</subject><subject>Baclofen - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Capsaicin</subject><subject>Capsaicin - antagonists & inhibitors</subject><subject>Drug Interactions - physiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>GABA Agonists - pharmacology</subject><subject>GABA Antagonists - pharmacology</subject><subject>GABA-B Receptor Agonists</subject><subject>GABA-B Receptor Antagonists</subject><subject>Injuries of the nervous system and the skull. Diseases due to physical agents</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Narcotic Antagonists - pharmacology</subject><subject>Neural Inhibition - drug effects</subject><subject>Neural Inhibition - physiology</subject><subject>Nucleus accumbens</subject><subject>Pain - chemically induced</subject><subject>Pain - physiopathology</subject><subject>Pain Threshold - drug effects</subject><subject>Pain Threshold - physiology</subject><subject>Pain-induced analgesia</subject><subject>Peptides - pharmacology</subject><subject>Rat</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, GABA-B - metabolism</subject><subject>Receptors, Opioid, mu - antagonists & inhibitors</subject><subject>Receptors, Opioid, mu - metabolism</subject><subject>Sensory System Agents - antagonists & inhibitors</subject><subject>Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors</subject><subject>Spinal cord</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - physiology</subject><subject>Synapses - drug effects</subject><subject>Synapses - physiology</subject><subject>Synaptic Transmission - drug effects</subject><subject>Synaptic Transmission - physiology</subject><subject>Traumas. Diseases due to physical agents</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0304-3959</issn><issn>1872-6623</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9UUtvEzEQXiEQTQt_gAPyBQkOG8aPdWIJVaoiHpUqOABny-v1NhM2dmR7U4L643G0UYELB8uy53vMzFdVLyjMKVD5djPfGfRzBqDmwOcAzaNqRpcLVkvJ-ONqBhxEzVWjzqrzlDYAwBhTT6szqviiYayZVfcr53M0A_4yGYMnoSc-_MQwJpIybsdhTDX6brSuI8ab4dYlNOT156_XV28IJhLdYHKp5UCMzbjHfCAmE_RrbDGHeCDp4M0uuVT-SF47knZYdIgNsXtWPenNkNzz031Rff_w_tvqU33z5eP16uqmto0SoqYNd8qCKFNB6RzEksq2ayQ3nYC2k9zapeUALVDHQPU9F2K56NyiU0ApbflFdTnp7sZ26zo7jax3EbcmHnQwqP-teFzr27DXTCrOZFME2CRgY0gpuv6BS0Efs9AbfcxCH7PQwHXJopBe_u36h3JafgG8OgFMsmboo_EW0wOOlblFQ1nBiQl3F4bsYvoxjHcu6rUzQ14XKwDJlayP3iDLqy6HikJ7N9FcWe0eCyNZdL4kidHZrLuA_2v_N-VnuaQ</recordid><startdate>20090601</startdate><enddate>20090601</enddate><creator>Tambeli, Claudia H.</creator><creator>Levine, Jon D.</creator><creator>Gear, Robert W.</creator><general>Elsevier B.V</general><general>Lippincott Williams & Wilkins, Inc</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>5PM</scope></search><sort><creationdate>20090601</creationdate><title>Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord</title><author>Tambeli, Claudia H. ; Levine, Jon D. ; Gear, Robert W.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5944-153e9c04662019304816bd563ad40bd63cc8c300b01e209ff34487de7d90111b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Analgesics - antagonists & inhibitors</topic><topic>Animals</topic><topic>Antinociception</topic><topic>Baclofen - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Capsaicin</topic><topic>Capsaicin - antagonists & inhibitors</topic><topic>Drug Interactions - physiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>GABA Agonists - pharmacology</topic><topic>GABA Antagonists - pharmacology</topic><topic>GABA-B Receptor Agonists</topic><topic>GABA-B Receptor Antagonists</topic><topic>Injuries of the nervous system and the skull. Diseases due to physical agents</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Narcotic Antagonists - pharmacology</topic><topic>Neural Inhibition - drug effects</topic><topic>Neural Inhibition - physiology</topic><topic>Nucleus accumbens</topic><topic>Pain - chemically induced</topic><topic>Pain - physiopathology</topic><topic>Pain Threshold - drug effects</topic><topic>Pain Threshold - physiology</topic><topic>Pain-induced analgesia</topic><topic>Peptides - pharmacology</topic><topic>Rat</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptors, GABA-B - metabolism</topic><topic>Receptors, Opioid, mu - antagonists & inhibitors</topic><topic>Receptors, Opioid, mu - metabolism</topic><topic>Sensory System Agents - antagonists & inhibitors</topic><topic>Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors</topic><topic>Spinal cord</topic><topic>Spinal Cord - drug effects</topic><topic>Spinal Cord - physiology</topic><topic>Synapses - drug effects</topic><topic>Synapses - physiology</topic><topic>Synaptic Transmission - drug effects</topic><topic>Synaptic Transmission - physiology</topic><topic>Traumas. Diseases due to physical agents</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tambeli, Claudia H.</creatorcontrib><creatorcontrib>Levine, Jon D.</creatorcontrib><creatorcontrib>Gear, Robert W.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Pain (Amsterdam)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tambeli, Claudia H.</au><au>Levine, Jon D.</au><au>Gear, Robert W.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord</atitle><jtitle>Pain (Amsterdam)</jtitle><addtitle>Pain</addtitle><date>2009-06-01</date><risdate>2009</risdate><volume>143</volume><issue>3</issue><spage>228</spage><epage>232</epage><pages>228-232</pages><issn>0304-3959</issn><eissn>1872-6623</eissn><coden>PAINDB</coden><abstract>The duration of noxious stimulus-induced antinociception (NSIA) has been shown to outlast the pain stimulus that elicited it, however, the mechanism that determines the duration of analgesia is unknown. We evaluated the role of spinal excitatory and inhibitory receptors (NMDA, mGluR5, μ-opioid, GABAA, and GABAB), previously implicated in NSIA initiation, in its maintenance. As in our previous studies, the supraspinal trigeminal jaw-opening reflex (JOR) in the rat was used for nociceptive testing because of its remoteness from the region of drug application, the lumbar spinal cord. NSIA was reversed by antagonists for two inhibitory receptors (GABAB and μ-opioid) but not by antagonists for either of the two excitatory receptors (NMDA and mGluR5), indicating that NSIA is maintained by ongoing activity at inhibitory synapses in the spinal cord. Furthermore, spinal administration of the GABAB agonist baclofen mimicked NSIA in that it could be blocked by prior injection of the μ-opioid receptor antagonist H-D-Phe-Cys-Tyr-D-Trp-Arg-Thr-Pen-Thr-NH2 (CTAP) in nucleus accumbens. CTAP also blocked baclofen antinociception when administered in the spinal cord. We conclude that analgesia induced by noxious stimulation is maintained by activity in spinal inhibitory receptors.</abstract><cop>Philadelphia, PA</cop><pub>Elsevier B.V</pub><pmid>19375225</pmid><doi>10.1016/j.pain.2009.03.005</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Pain (Amsterdam), 2009-06, Vol.143 (3), p.228-232 |
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| subjects | Analgesics - antagonists & inhibitors Animals Antinociception Baclofen - pharmacology Biological and medical sciences Capsaicin Capsaicin - antagonists & inhibitors Drug Interactions - physiology Fundamental and applied biological sciences. Psychology GABA Agonists - pharmacology GABA Antagonists - pharmacology GABA-B Receptor Agonists GABA-B Receptor Antagonists Injuries of the nervous system and the skull. Diseases due to physical agents Male Medical sciences Narcotic Antagonists - pharmacology Neural Inhibition - drug effects Neural Inhibition - physiology Nucleus accumbens Pain - chemically induced Pain - physiopathology Pain Threshold - drug effects Pain Threshold - physiology Pain-induced analgesia Peptides - pharmacology Rat Rats Rats, Sprague-Dawley Receptors, GABA-B - metabolism Receptors, Opioid, mu - antagonists & inhibitors Receptors, Opioid, mu - metabolism Sensory System Agents - antagonists & inhibitors Somesthesis and somesthetic pathways (proprioception, exteroception, nociception) interoception electrolocation. Sensory receptors Spinal cord Spinal Cord - drug effects Spinal Cord - physiology Synapses - drug effects Synapses - physiology Synaptic Transmission - drug effects Synaptic Transmission - physiology Traumas. Diseases due to physical agents Vertebrates: nervous system and sense organs |
| title | Centralization of noxious stimulus-induced analgesia (NSIA) is related to activity at inhibitory synapses in the spinal cord |
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