Ethanol-Induced Antinociception in Rodents: Role of the Cholinergic and Opioidergic Systems
We examined antinociceptive properties of ethanol and the mechanism of its action using two thermal (hot-plate and tail-flick) and two chemical (acetic acid-induced writhing and formalin) nociception tests. The mechanism of antinociception was analyzed using naloxone (an opioid antagonist) and atrop...
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Veröffentlicht in: | Neurophysiology (New York) 2012-12, Vol.44 (6), p.460-463 |
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description | We examined antinociceptive properties of ethanol and the mechanism of its action using two thermal (hot-plate and tail-flick) and two chemical (acetic acid-induced writhing and formalin) nociception tests. The mechanism of antinociception was analyzed using naloxone (an opioid antagonist) and atropine (a cholinergic blocker). It was found that ethanol in a dose-dependent manner produced significant (
P
< < 0.05) prolongations of both the hot-plate and tail-flick latencies. In the chemical tests, ethanol caused a significant (
P
< 0.05) reduction in the number of writhings produced by acetic acid and also a significant decrease (
P
< 0.01) in the licking time produced by formalin within both phases of the respective test. It was also observed that both atropine and naloxone significantly (
P
< 0.05) suppressed ethanolinduced antinociception effects. We conclude that the antinociceptive action of ethanol may in part be opiodergic- and cholinergic-dependent. |
doi_str_mv | 10.1007/s11062-012-9318-5 |
format | Article |
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P
< < 0.05) prolongations of both the hot-plate and tail-flick latencies. In the chemical tests, ethanol caused a significant (
P
< 0.05) reduction in the number of writhings produced by acetic acid and also a significant decrease (
P
< 0.01) in the licking time produced by formalin within both phases of the respective test. It was also observed that both atropine and naloxone significantly (
P
< 0.05) suppressed ethanolinduced antinociception effects. We conclude that the antinociceptive action of ethanol may in part be opiodergic- and cholinergic-dependent.</description><identifier>ISSN: 0090-2977</identifier><identifier>EISSN: 1573-9007</identifier><identifier>DOI: 10.1007/s11062-012-9318-5</identifier><language>eng</language><publisher>Boston: Springer US</publisher><subject>Acetic acid ; Alcohol ; Alcohol, Denatured ; Analysis ; Biomedical and Life Sciences ; Biomedicine ; Ethanol ; Formaldehyde ; Neurobiology ; Neurosciences ; Organic acids ; Pain ; Rodents</subject><ispartof>Neurophysiology (New York), 2012-12, Vol.44 (6), p.460-463</ispartof><rights>Springer Science+Business Media New York 2012</rights><rights>COPYRIGHT 2012 Springer</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c450t-896817bd4d8d08e9aa91cb0712ac918574414efe47c8e082741cbc1ae3b614793</citedby><cites>FETCH-LOGICAL-c450t-896817bd4d8d08e9aa91cb0712ac918574414efe47c8e082741cbc1ae3b614793</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11062-012-9318-5$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11062-012-9318-5$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids></links><search><creatorcontrib>Ibironke, G. F.</creatorcontrib><creatorcontrib>Oyekunle, O. A.</creatorcontrib><title>Ethanol-Induced Antinociception in Rodents: Role of the Cholinergic and Opioidergic Systems</title><title>Neurophysiology (New York)</title><addtitle>Neurophysiology</addtitle><description>We examined antinociceptive properties of ethanol and the mechanism of its action using two thermal (hot-plate and tail-flick) and two chemical (acetic acid-induced writhing and formalin) nociception tests. The mechanism of antinociception was analyzed using naloxone (an opioid antagonist) and atropine (a cholinergic blocker). It was found that ethanol in a dose-dependent manner produced significant (
P
< < 0.05) prolongations of both the hot-plate and tail-flick latencies. In the chemical tests, ethanol caused a significant (
P
< 0.05) reduction in the number of writhings produced by acetic acid and also a significant decrease (
P
< 0.01) in the licking time produced by formalin within both phases of the respective test. It was also observed that both atropine and naloxone significantly (
P
< 0.05) suppressed ethanolinduced antinociception effects. We conclude that the antinociceptive action of ethanol may in part be opiodergic- and cholinergic-dependent.</description><subject>Acetic acid</subject><subject>Alcohol</subject><subject>Alcohol, Denatured</subject><subject>Analysis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Ethanol</subject><subject>Formaldehyde</subject><subject>Neurobiology</subject><subject>Neurosciences</subject><subject>Organic acids</subject><subject>Pain</subject><subject>Rodents</subject><issn>0090-2977</issn><issn>1573-9007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1kc9rHCEUx4fSQLdp_4DeBnppD6a-GWfU3pYlbRYCgfw45SCuvtk1zOpWHWj--7pMDtnS4kGf7_N5KN-q-gT0Aijl3xIA7RtCoSGyBUG6N9UCOt4SWbpvqwWlkpJGcv6uep_SE6W0F7JbVI-Xead9GMna28mgrZc-Ox-MM3jILvja-fo2WPQ5fS-HEesw1HmH9WoXRucxbp2ptbf1zcEFZ-f67jll3KcP1dmgx4QfX_bz6uHH5f3qilzf_FyvltfEsI5mImQvgG8ss8JSgVJrCWZDOTTaSBAdZwwYDsi4EUhFw1lpG9DYbnpgXLbn1Zd57iGGXxOmrPYuGRxH7TFMSQHrWVdI6Av6-S_0KUzRl9cVigku-469orZ6ROX8EHLU5jhULVvOBDSCt4W6-AdVlsW9M8Hj4Mr9ifD1RChMxt95q6eU1Pru9pSFmTUxpBRxUIfo9jo-K6DqmLiaE1clcXVMXHXFaWYnFdZvMb763H-lPx7PqoA</recordid><startdate>20121201</startdate><enddate>20121201</enddate><creator>Ibironke, G. 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F. ; Oyekunle, O. A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c450t-896817bd4d8d08e9aa91cb0712ac918574414efe47c8e082741cbc1ae3b614793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Acetic acid</topic><topic>Alcohol</topic><topic>Alcohol, Denatured</topic><topic>Analysis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Ethanol</topic><topic>Formaldehyde</topic><topic>Neurobiology</topic><topic>Neurosciences</topic><topic>Organic acids</topic><topic>Pain</topic><topic>Rodents</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ibironke, G. F.</creatorcontrib><creatorcontrib>Oyekunle, O. 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F.</au><au>Oyekunle, O. A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Ethanol-Induced Antinociception in Rodents: Role of the Cholinergic and Opioidergic Systems</atitle><jtitle>Neurophysiology (New York)</jtitle><stitle>Neurophysiology</stitle><date>2012-12-01</date><risdate>2012</risdate><volume>44</volume><issue>6</issue><spage>460</spage><epage>463</epage><pages>460-463</pages><issn>0090-2977</issn><eissn>1573-9007</eissn><abstract>We examined antinociceptive properties of ethanol and the mechanism of its action using two thermal (hot-plate and tail-flick) and two chemical (acetic acid-induced writhing and formalin) nociception tests. The mechanism of antinociception was analyzed using naloxone (an opioid antagonist) and atropine (a cholinergic blocker). It was found that ethanol in a dose-dependent manner produced significant (
P
< < 0.05) prolongations of both the hot-plate and tail-flick latencies. In the chemical tests, ethanol caused a significant (
P
< 0.05) reduction in the number of writhings produced by acetic acid and also a significant decrease (
P
< 0.01) in the licking time produced by formalin within both phases of the respective test. It was also observed that both atropine and naloxone significantly (
P
< 0.05) suppressed ethanolinduced antinociception effects. We conclude that the antinociceptive action of ethanol may in part be opiodergic- and cholinergic-dependent.</abstract><cop>Boston</cop><pub>Springer US</pub><doi>10.1007/s11062-012-9318-5</doi><tpages>4</tpages></addata></record> |
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subjects | Acetic acid Alcohol Alcohol, Denatured Analysis Biomedical and Life Sciences Biomedicine Ethanol Formaldehyde Neurobiology Neurosciences Organic acids Pain Rodents |
title | Ethanol-Induced Antinociception in Rodents: Role of the Cholinergic and Opioidergic Systems |
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