Utilize este identificador para referenciar este registo:
https://hdl.handle.net/1822/32930
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Campo DC | Valor | Idioma |
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dc.contributor.author | Wei, Hong | por |
dc.contributor.author | Viisanen, Hanna | por |
dc.contributor.author | Amorim, Diana | por |
dc.contributor.author | Koivisto, Ari | por |
dc.contributor.author | Pertovaara, Antti | por |
dc.date.accessioned | 2015-01-16T15:01:23Z | - |
dc.date.available | 2015-01-16T15:01:23Z | - |
dc.date.issued | 2013 | - |
dc.identifier.issn | 0091-3057 | por |
dc.identifier.uri | https://hdl.handle.net/1822/32930 | - |
dc.description | Uncorrected proof | por |
dc.description.abstract | Transient receptor potential ankyrin 1 (TRPA1) channel antagonists have suppressed mechanical hypersensitivity in peripheral neuropathy, while their effect on ongoing neuropathic pain is not yet known. Here, we assessed whether blocking the TRPA1 channel induces place-preference, an index for the relief of ongoing pain, in two experimental rat models of peripheral neuropathy. Diabetic neuropathy was induced by streptozotocin and spared nerve injury (SNI) model of neuropathy by ligation of two sciatic nerve branches. Conditioned place-preference (CPP) paradigm involved pairing of the drug treatment with one of the chambers of a CPP device once or four times, and the time spent in each chamber was recorded after conditioning sessions to reveal place-preference. The mechanical antihypersensitivity effect was assessed by the monofilament test immediately after the conditioning sessions. Intraperitoneally (30mg/kg; diabetic and SNI model) or intrathecally (10µg; diabetic model) administered Chembridge-5861528 (CHEM) was used as a selective TRPA1 channel antagonist. In diabetic and SNI models of neuropathy, CHEM failed to induce CPP at a dose that significantly attenuated mechanical hypersensitivity, independent of the route of drug administration or number of successive conditioning sessions. Intrathecal clonidine (an a2-adrenoceptor agonist; 10µg), in contrast, induced CPP in SNI but not control animals. The results indicate that ongoing pain, as revealed by CPP, is less sensitive to treatment by the TRPA1 channel antagonist than mechanical hypersensitivity in peripheral neuropathy. | por |
dc.description.sponsorship | One of the authors (A.K.) is an employee of the pharmaceutical company (OrionPharma, Finland) that has supported this study.The study was supported by the Sigrid Juselius Foundation, Helsinki, the Academy of Finland, Helsinki, and OrionPharma, Orion Corporation, Turku, Finland. Diana Amorim was supported by the Portuguese Science Foundation (FCT) grant SFRH/BD/71219/2010. | por |
dc.language.iso | eng | por |
dc.publisher | Elsevier 1 | por |
dc.rights | openAccess | por |
dc.subject | Chembridge-5861528 | por |
dc.subject | Clonidine | por |
dc.subject | Conditioned place-preference | por |
dc.subject | Diabetic neuropathy | por |
dc.subject | Mechanical hypersensitivity | por |
dc.subject | Ongoing pain | por |
dc.subject | Peripheral nerve injury | por |
dc.subject | Transient receptor potential ankyrin 1 channel | por |
dc.title | Dissociated modulation of conditioned place-preference and mechanical hypersensitivity by a TRPA1 channel antagonist in peripheral neuropathy | por |
dc.type | article | - |
dc.peerreviewed | yes | por |
dc.relation.publisherversion | www.elsevier.com | por |
sdum.publicationstatus | published | por |
oaire.citationStartPage | 90 | por |
oaire.citationEndPage | 96 | por |
oaire.citationIssue | 1 | por |
oaire.citationTitle | Pharmacology Biochemistry and Behavior | por |
oaire.citationVolume | 104 | por |
dc.date.updated | 2015-01-13T17:17:58Z | - |
dc.identifier.doi | 10.1016/j.pbb.2012.12.014 | por |
dc.identifier.pmid | 23287802 | por |
dc.subject.wos | Science & Technology | por |
sdum.journal | Pharmacology Biochemistry and Behavior | por |
Aparece nas coleções: | ICVS - Artigos em revistas internacionais / Papers in international journals |
Ficheiros deste registo:
Ficheiro | Descrição | Tamanho | Formato | |
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wei hong_pharmbiochembehav 2013 pp.pdf | 751,71 kB | Adobe PDF | Ver/Abrir |