Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats
► We explore pathophysiology of fibromyalgia-like reserpine-induced myalgia rat model. ► Degenerative changes at the level of primary afferents and spinal cord are not responsible for pain symptoms. ► A sodium channel blocker does not reduce hyperalgesia. ► Dysfunctional brain pain control is involv...
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| creator | Nagakura, Yukinori Takahashi, Masayasu Noto, Takahisa Sekizawa, Toshihiro Oe, Tomoya Yoshimi, Eiji Tamaki, Keisuke Shimizu, Yasuaki |
| description | ► We explore pathophysiology of fibromyalgia-like reserpine-induced myalgia rat model. ► Degenerative changes at the level of primary afferents and spinal cord are not responsible for pain symptoms. ► A sodium channel blocker does not reduce hyperalgesia. ► Dysfunctional brain pain control is involved in the pathophysiology. ► Pathophysiology of the model is distinct from that for the neuropathic pain state.
The reserpine-induced myalgia (RIM) rat manifests fibromyalgia-like chronic pain symptoms. The present study explored the pathophysiology underlying the pain symptoms in the RIM rat and the chronic constriction injury (CCI) rat, an animal model of neuropathic pain as a reference. Nerve tissue samples were collected from the nociception-tested animals for pathological examinations. Additionally, the therapeutic efficacy of a sodium channel blocker mexiletine was assessed in both rats. A slight vacuolization in the substantia nigra (SN) occurred in some of the RIM rats without any other histopathological changes in the brain or peripheral neurons. All the RIM rats, with or without vacuolization, showed hypersensitivity to tactile, muscle pressure, and cold stimuli. In the CCI rat, neurodegenerative changes were apparent in the sciatic nerve and the spinal cord only. CCI rats displayed muscle hyperalgesia in addition to tactile and cold allodynia. Pharmacotherapy with mexiletine did not attenuate the pain in the RIM rat, although it was effective in the CCI rat. Taken together, it is not likely that pain symptoms in RIM rats are caused by degenerative changes at the level of primary afferents and spinal cord, as is the case for CCI rats. The significance of the vacuolization in the SN is less clear at present because of the minor extent of the change and the lack of correlation with nociceptive sensitivity. The pain symptoms in RIM rats could be associated with dysfunction of biogenic amines-mediated CNS pain control even without apparent pathologies in the nervous system. |
| doi_str_mv | 10.1016/j.bbr.2011.09.023 |
| format | Article |
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The reserpine-induced myalgia (RIM) rat manifests fibromyalgia-like chronic pain symptoms. The present study explored the pathophysiology underlying the pain symptoms in the RIM rat and the chronic constriction injury (CCI) rat, an animal model of neuropathic pain as a reference. Nerve tissue samples were collected from the nociception-tested animals for pathological examinations. Additionally, the therapeutic efficacy of a sodium channel blocker mexiletine was assessed in both rats. A slight vacuolization in the substantia nigra (SN) occurred in some of the RIM rats without any other histopathological changes in the brain or peripheral neurons. All the RIM rats, with or without vacuolization, showed hypersensitivity to tactile, muscle pressure, and cold stimuli. In the CCI rat, neurodegenerative changes were apparent in the sciatic nerve and the spinal cord only. CCI rats displayed muscle hyperalgesia in addition to tactile and cold allodynia. Pharmacotherapy with mexiletine did not attenuate the pain in the RIM rat, although it was effective in the CCI rat. Taken together, it is not likely that pain symptoms in RIM rats are caused by degenerative changes at the level of primary afferents and spinal cord, as is the case for CCI rats. The significance of the vacuolization in the SN is less clear at present because of the minor extent of the change and the lack of correlation with nociceptive sensitivity. The pain symptoms in RIM rats could be associated with dysfunction of biogenic amines-mediated CNS pain control even without apparent pathologies in the nervous system.</description><identifier>ISSN: 0166-4328</identifier><identifier>EISSN: 1872-7549</identifier><identifier>DOI: 10.1016/j.bbr.2011.09.023</identifier><identifier>PMID: 21945299</identifier><identifier>CODEN: BBREDI</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Animals ; Behavioral psychophysiology ; Biological and medical sciences ; Chronic Pain ; Constriction ; Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction ; Disease Models, Animal ; Diseases of the osteoarticular system ; Fibromyalgia ; Fibromyalgia - chemically induced ; Fibromyalgia - physiopathology ; Fundamental and applied biological sciences. Psychology ; Hyperalgesia - etiology ; Hyperalgesia - physiopathology ; Male ; Medical sciences ; Miscellaneous. Osteoarticular involvement in other diseases ; Nervous system (semeiology, syndromes) ; Neuralgia - etiology ; Neuralgia - physiopathology ; Neurology ; Neuropathic pain ; Neuropharmacology ; Pharmacology. Drug treatments ; Physical Stimulation ; Psycholeptics: tranquillizer, neuroleptic ; Psychology. Psychoanalysis. Psychiatry ; Psychology. Psychophysiology ; Psychopharmacology ; Rats ; Rats, Sprague-Dawley ; Reserpine - pharmacology ; Reserpine-induced myalgia ; Sciatic Nerve - injuries ; Sciatic Nerve - physiopathology ; Sodium channel blocker ; Substantia nigra</subject><ispartof>Behavioural brain research, 2012, Vol.226 (1), p.242-249</ispartof><rights>2011 Elsevier B.V.</rights><rights>2015 INIST-CNRS</rights><rights>Copyright © 2011 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c480t-6de3cb7d56b26d12ee0eaf50fb13f0735fc2d61ae8aeb70ea3feaac13e1989e23</citedby><cites>FETCH-LOGICAL-c480t-6de3cb7d56b26d12ee0eaf50fb13f0735fc2d61ae8aeb70ea3feaac13e1989e23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbr.2011.09.023$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,4024,27923,27924,27925,45995</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=24703895$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21945299$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Nagakura, Yukinori</creatorcontrib><creatorcontrib>Takahashi, Masayasu</creatorcontrib><creatorcontrib>Noto, Takahisa</creatorcontrib><creatorcontrib>Sekizawa, Toshihiro</creatorcontrib><creatorcontrib>Oe, Tomoya</creatorcontrib><creatorcontrib>Yoshimi, Eiji</creatorcontrib><creatorcontrib>Tamaki, Keisuke</creatorcontrib><creatorcontrib>Shimizu, Yasuaki</creatorcontrib><title>Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats</title><title>Behavioural brain research</title><addtitle>Behav Brain Res</addtitle><description>► We explore pathophysiology of fibromyalgia-like reserpine-induced myalgia rat model. ► Degenerative changes at the level of primary afferents and spinal cord are not responsible for pain symptoms. ► A sodium channel blocker does not reduce hyperalgesia. ► Dysfunctional brain pain control is involved in the pathophysiology. ► Pathophysiology of the model is distinct from that for the neuropathic pain state.
The reserpine-induced myalgia (RIM) rat manifests fibromyalgia-like chronic pain symptoms. The present study explored the pathophysiology underlying the pain symptoms in the RIM rat and the chronic constriction injury (CCI) rat, an animal model of neuropathic pain as a reference. Nerve tissue samples were collected from the nociception-tested animals for pathological examinations. Additionally, the therapeutic efficacy of a sodium channel blocker mexiletine was assessed in both rats. A slight vacuolization in the substantia nigra (SN) occurred in some of the RIM rats without any other histopathological changes in the brain or peripheral neurons. All the RIM rats, with or without vacuolization, showed hypersensitivity to tactile, muscle pressure, and cold stimuli. In the CCI rat, neurodegenerative changes were apparent in the sciatic nerve and the spinal cord only. CCI rats displayed muscle hyperalgesia in addition to tactile and cold allodynia. Pharmacotherapy with mexiletine did not attenuate the pain in the RIM rat, although it was effective in the CCI rat. Taken together, it is not likely that pain symptoms in RIM rats are caused by degenerative changes at the level of primary afferents and spinal cord, as is the case for CCI rats. The significance of the vacuolization in the SN is less clear at present because of the minor extent of the change and the lack of correlation with nociceptive sensitivity. The pain symptoms in RIM rats could be associated with dysfunction of biogenic amines-mediated CNS pain control even without apparent pathologies in the nervous system.</description><subject>Animals</subject><subject>Behavioral psychophysiology</subject><subject>Biological and medical sciences</subject><subject>Chronic Pain</subject><subject>Constriction</subject><subject>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</subject><subject>Disease Models, Animal</subject><subject>Diseases of the osteoarticular system</subject><subject>Fibromyalgia</subject><subject>Fibromyalgia - chemically induced</subject><subject>Fibromyalgia - physiopathology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hyperalgesia - etiology</subject><subject>Hyperalgesia - physiopathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Miscellaneous. Osteoarticular involvement in other diseases</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neuralgia - etiology</subject><subject>Neuralgia - physiopathology</subject><subject>Neurology</subject><subject>Neuropathic pain</subject><subject>Neuropharmacology</subject><subject>Pharmacology. Drug treatments</subject><subject>Physical Stimulation</subject><subject>Psycholeptics: tranquillizer, neuroleptic</subject><subject>Psychology. Psychoanalysis. Psychiatry</subject><subject>Psychology. Psychophysiology</subject><subject>Psychopharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reserpine - pharmacology</subject><subject>Reserpine-induced myalgia</subject><subject>Sciatic Nerve - injuries</subject><subject>Sciatic Nerve - physiopathology</subject><subject>Sodium channel blocker</subject><subject>Substantia nigra</subject><issn>0166-4328</issn><issn>1872-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkbuu1DAQhiME4iwHHoAGuUFUWXzJzVCh5SodiQZqy7HHu7NK7GAnSHkg3hNHu1wqROVivu8fa_6ieMronlHWvDzv-z7uOWVsT-WecnGv2LGu5WVbV_J-sctMU1aCdzfFo5TOlNKK1uxhccOZrGou5a748Radgwh-JpOeT2E6rQnDEI4rWbyFOKzoj0R7HPVAxmBhSCQ44rCPYVz1cESdp5Z4WGLYEtDkIPSvyCGMk46Ygt-ECAnihB5K9HYxYMnftjnF4LNpgk9zRDNjttCfl7iSqOf0uHjg9JDgyfW9Lb6-f_fl8LG8-_zh0-HNXWmqjs5lY0GYvrV10_PGMg5AQbuaup4JR1tRO8NtwzR0Gvo2z4QDrQ0TwGQngYvb4sUld4rh2wJpViMmA8OgPYQlKZlv3NaMif8gacOrhm4ku5AmhpQiODXFfM24KkbVVqM6q1yj2mpUVKq8IjvPrulLP4L9bfzqLQPPr4BORg8uam8w_eGqlopO1pl7feFyb_AdIapkEHy-P0Yws7IB__GNn2ipwF8</recordid><startdate>2012</startdate><enddate>2012</enddate><creator>Nagakura, Yukinori</creator><creator>Takahashi, Masayasu</creator><creator>Noto, Takahisa</creator><creator>Sekizawa, Toshihiro</creator><creator>Oe, Tomoya</creator><creator>Yoshimi, Eiji</creator><creator>Tamaki, Keisuke</creator><creator>Shimizu, Yasuaki</creator><general>Elsevier B.V</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>7X8</scope><scope>7QG</scope><scope>7TK</scope></search><sort><creationdate>2012</creationdate><title>Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats</title><author>Nagakura, Yukinori ; Takahashi, Masayasu ; Noto, Takahisa ; Sekizawa, Toshihiro ; Oe, Tomoya ; Yoshimi, Eiji ; Tamaki, Keisuke ; Shimizu, Yasuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c480t-6de3cb7d56b26d12ee0eaf50fb13f0735fc2d61ae8aeb70ea3feaac13e1989e23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Animals</topic><topic>Behavioral psychophysiology</topic><topic>Biological and medical sciences</topic><topic>Chronic Pain</topic><topic>Constriction</topic><topic>Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction</topic><topic>Disease Models, Animal</topic><topic>Diseases of the osteoarticular system</topic><topic>Fibromyalgia</topic><topic>Fibromyalgia - chemically induced</topic><topic>Fibromyalgia - physiopathology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hyperalgesia - etiology</topic><topic>Hyperalgesia - physiopathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Miscellaneous. Osteoarticular involvement in other diseases</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neuralgia - etiology</topic><topic>Neuralgia - physiopathology</topic><topic>Neurology</topic><topic>Neuropathic pain</topic><topic>Neuropharmacology</topic><topic>Pharmacology. Drug treatments</topic><topic>Physical Stimulation</topic><topic>Psycholeptics: tranquillizer, neuroleptic</topic><topic>Psychology. Psychoanalysis. Psychiatry</topic><topic>Psychology. Psychophysiology</topic><topic>Psychopharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reserpine - pharmacology</topic><topic>Reserpine-induced myalgia</topic><topic>Sciatic Nerve - injuries</topic><topic>Sciatic Nerve - physiopathology</topic><topic>Sodium channel blocker</topic><topic>Substantia nigra</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Nagakura, Yukinori</creatorcontrib><creatorcontrib>Takahashi, Masayasu</creatorcontrib><creatorcontrib>Noto, Takahisa</creatorcontrib><creatorcontrib>Sekizawa, Toshihiro</creatorcontrib><creatorcontrib>Oe, Tomoya</creatorcontrib><creatorcontrib>Yoshimi, Eiji</creatorcontrib><creatorcontrib>Tamaki, Keisuke</creatorcontrib><creatorcontrib>Shimizu, Yasuaki</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>MEDLINE - Academic</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Behavioural brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Nagakura, Yukinori</au><au>Takahashi, Masayasu</au><au>Noto, Takahisa</au><au>Sekizawa, Toshihiro</au><au>Oe, Tomoya</au><au>Yoshimi, Eiji</au><au>Tamaki, Keisuke</au><au>Shimizu, Yasuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats</atitle><jtitle>Behavioural brain research</jtitle><addtitle>Behav Brain Res</addtitle><date>2012</date><risdate>2012</risdate><volume>226</volume><issue>1</issue><spage>242</spage><epage>249</epage><pages>242-249</pages><issn>0166-4328</issn><eissn>1872-7549</eissn><coden>BBREDI</coden><abstract>► We explore pathophysiology of fibromyalgia-like reserpine-induced myalgia rat model. ► Degenerative changes at the level of primary afferents and spinal cord are not responsible for pain symptoms. ► A sodium channel blocker does not reduce hyperalgesia. ► Dysfunctional brain pain control is involved in the pathophysiology. ► Pathophysiology of the model is distinct from that for the neuropathic pain state.
The reserpine-induced myalgia (RIM) rat manifests fibromyalgia-like chronic pain symptoms. The present study explored the pathophysiology underlying the pain symptoms in the RIM rat and the chronic constriction injury (CCI) rat, an animal model of neuropathic pain as a reference. Nerve tissue samples were collected from the nociception-tested animals for pathological examinations. Additionally, the therapeutic efficacy of a sodium channel blocker mexiletine was assessed in both rats. A slight vacuolization in the substantia nigra (SN) occurred in some of the RIM rats without any other histopathological changes in the brain or peripheral neurons. All the RIM rats, with or without vacuolization, showed hypersensitivity to tactile, muscle pressure, and cold stimuli. In the CCI rat, neurodegenerative changes were apparent in the sciatic nerve and the spinal cord only. CCI rats displayed muscle hyperalgesia in addition to tactile and cold allodynia. Pharmacotherapy with mexiletine did not attenuate the pain in the RIM rat, although it was effective in the CCI rat. Taken together, it is not likely that pain symptoms in RIM rats are caused by degenerative changes at the level of primary afferents and spinal cord, as is the case for CCI rats. The significance of the vacuolization in the SN is less clear at present because of the minor extent of the change and the lack of correlation with nociceptive sensitivity. The pain symptoms in RIM rats could be associated with dysfunction of biogenic amines-mediated CNS pain control even without apparent pathologies in the nervous system.</abstract><cop>Shannon</cop><pub>Elsevier B.V</pub><pmid>21945299</pmid><doi>10.1016/j.bbr.2011.09.023</doi><tpages>8</tpages></addata></record> |
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| ispartof | Behavioural brain research, 2012, Vol.226 (1), p.242-249 |
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| subjects | Animals Behavioral psychophysiology Biological and medical sciences Chronic Pain Constriction Cranial nerves. Spinal roots. Peripheral nerves. Autonomic nervous system. Gustation. Olfaction Disease Models, Animal Diseases of the osteoarticular system Fibromyalgia Fibromyalgia - chemically induced Fibromyalgia - physiopathology Fundamental and applied biological sciences. Psychology Hyperalgesia - etiology Hyperalgesia - physiopathology Male Medical sciences Miscellaneous. Osteoarticular involvement in other diseases Nervous system (semeiology, syndromes) Neuralgia - etiology Neuralgia - physiopathology Neurology Neuropathic pain Neuropharmacology Pharmacology. Drug treatments Physical Stimulation Psycholeptics: tranquillizer, neuroleptic Psychology. Psychoanalysis. Psychiatry Psychology. Psychophysiology Psychopharmacology Rats Rats, Sprague-Dawley Reserpine - pharmacology Reserpine-induced myalgia Sciatic Nerve - injuries Sciatic Nerve - physiopathology Sodium channel blocker Substantia nigra |
| title | Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats |
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