Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats
Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxid...
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| Veröffentlicht in: | BMC neuroscience 2013-08, Vol.14 (1), p.92-92, Article 92 |
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| creator | Damasceno, Fabio Skinner, Gabriela O Araújo, Paulo C Ferraz, Marcia M D Tenório, Frank de Almeida, Olga M M S |
| description | Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxide (NO) and the dorsolateral periaqueductal gray matter (dlPAG) area of the brainstem are involved in hyperalgesia. Thus, in this work, we investigated the pain-related behavior response after mechanical noxious stimuli (electronic von Frey test), and the activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an indicator of NOS activity, within the dlPAG of paradoxical sleep-deprived rats. We also evaluated the effects of pre-treatment with L-NAME on these parameters.
These data revealed that PSD reduced the hindpaw withdrawal threshold (-47%, p |
| doi_str_mv | 10.1186/1471-2202-14-92 |
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These data revealed that PSD reduced the hindpaw withdrawal threshold (-47%, p < 0.0001) confirming the hyperalgesic effect of this condition. In addition, there were more NADPH-d positive cells in dlPAG after PSD than in control rats (+ 59%, p < 0.0001). L-NAME treatment prevented the reduction in the hindpaw withdrawal threshold (+ 93%, p < 0.0001) and the increase in the NADPH-d positive cells number in the dlPAG of PSD-treated rats (-36%, p < 0.0001).
These data suggest that the hyperalgesic response to mechanical noxious stimuli in paradoxical sleep-deprived rats is associated with increased NOS activity in the dlPAG, which presumably influences the descending antinociceptive pathway.</description><identifier>ISSN: 1471-2202</identifier><identifier>EISSN: 1471-2202</identifier><identifier>DOI: 10.1186/1471-2202-14-92</identifier><identifier>PMID: 23987566</identifier><language>eng</language><publisher>England: BioMed Central Ltd</publisher><subject>Animals ; Health aspects ; Hyperalgesia - metabolism ; Kinases ; Male ; Nitric oxide ; Nitric Oxide - metabolism ; Pain ; Periaqueductal Gray - metabolism ; Physical Stimulation ; Rats ; Rats, Wistar ; Rodents ; Sleep deprivation ; Sleep Deprivation - metabolism</subject><ispartof>BMC neuroscience, 2013-08, Vol.14 (1), p.92-92, Article 92</ispartof><rights>COPYRIGHT 2013 BioMed Central Ltd.</rights><rights>2013 Damasceno et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2013 Damasceno et al.; licensee BioMed Central Ltd. 2013 Damasceno et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b580t-65d17d1f390bc6a8892603c7351db5a6962f648f506670b602af71a931d60d033</citedby><cites>FETCH-LOGICAL-b580t-65d17d1f390bc6a8892603c7351db5a6962f648f506670b602af71a931d60d033</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765713/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3765713/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/23987566$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Damasceno, Fabio</creatorcontrib><creatorcontrib>Skinner, Gabriela O</creatorcontrib><creatorcontrib>Araújo, Paulo C</creatorcontrib><creatorcontrib>Ferraz, Marcia M D</creatorcontrib><creatorcontrib>Tenório, Frank</creatorcontrib><creatorcontrib>de Almeida, Olga M M S</creatorcontrib><title>Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats</title><title>BMC neuroscience</title><addtitle>BMC Neurosci</addtitle><description>Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxide (NO) and the dorsolateral periaqueductal gray matter (dlPAG) area of the brainstem are involved in hyperalgesia. Thus, in this work, we investigated the pain-related behavior response after mechanical noxious stimuli (electronic von Frey test), and the activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an indicator of NOS activity, within the dlPAG of paradoxical sleep-deprived rats. We also evaluated the effects of pre-treatment with L-NAME on these parameters.
These data revealed that PSD reduced the hindpaw withdrawal threshold (-47%, p < 0.0001) confirming the hyperalgesic effect of this condition. In addition, there were more NADPH-d positive cells in dlPAG after PSD than in control rats (+ 59%, p < 0.0001). L-NAME treatment prevented the reduction in the hindpaw withdrawal threshold (+ 93%, p < 0.0001) and the increase in the NADPH-d positive cells number in the dlPAG of PSD-treated rats (-36%, p < 0.0001).
These data suggest that the hyperalgesic response to mechanical noxious stimuli in paradoxical sleep-deprived rats is associated with increased NOS activity in the dlPAG, which presumably influences the descending antinociceptive pathway.</description><subject>Animals</subject><subject>Health aspects</subject><subject>Hyperalgesia - metabolism</subject><subject>Kinases</subject><subject>Male</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Pain</subject><subject>Periaqueductal Gray - metabolism</subject><subject>Physical Stimulation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Rodents</subject><subject>Sleep deprivation</subject><subject>Sleep Deprivation - metabolism</subject><issn>1471-2202</issn><issn>1471-2202</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkstv1DAQxiMEog84c0OWuHBJ60f8yAWpVFCQKrjA2XLsya6rxA52UtH_Hkdbli4qEvLBo5nffBp_nqp6RfAZIUqck0aSmlJMa9LULX1SHe8zTx_ER9VJzjcYE6ka-rw6oqxVkgtxXMEXPydvUfzpHaAxumUwM2Q0bwFt7yZIZthALkCCPMWQAc0RjWC3JnhrBhRKY1wyyrMfl8EjH1AeAKbawZT8LTiUzJxfVM96M2R4eX-fVt8_fvh2-am-_nr1-fLiuu64wnMtuCPSkZ61uLPCKNVSgZmVjBPXcSNaQXvRqJ5jISTuBKaml8S0jDiBHWbstHq3052WbgRnIczlAbpMMpp0p6Px-rAS_FZv4q1mUnBJVoH3O4HOx38IHFZsHPVqs15tLpFuaRF5ez9Fij8WyLMefbYwDCZA8apQvCWcUiX_A2UNZgTLdbQ3f6E3cUmh2Fko2nIqSaP-UBszgPahj2VMu4rqC84aLpkiolBnj1DlOBi9jQF6X_IHDee7Bptizgn6vSUE63UTHzHh9cOv2PO_V4_9AvQU2B8</recordid><startdate>20130830</startdate><enddate>20130830</enddate><creator>Damasceno, Fabio</creator><creator>Skinner, Gabriela O</creator><creator>Araújo, Paulo C</creator><creator>Ferraz, Marcia M D</creator><creator>Tenório, Frank</creator><creator>de Almeida, Olga M M S</creator><general>BioMed Central Ltd</general><general>BioMed Central</general><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>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20130830</creationdate><title>Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats</title><author>Damasceno, Fabio ; Skinner, Gabriela O ; Araújo, Paulo C ; Ferraz, Marcia M D ; Tenório, Frank ; de Almeida, Olga M M S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-b580t-65d17d1f390bc6a8892603c7351db5a6962f648f506670b602af71a931d60d033</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Animals</topic><topic>Health aspects</topic><topic>Hyperalgesia - metabolism</topic><topic>Kinases</topic><topic>Male</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Pain</topic><topic>Periaqueductal Gray - metabolism</topic><topic>Physical Stimulation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Rodents</topic><topic>Sleep deprivation</topic><topic>Sleep Deprivation - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Damasceno, Fabio</creatorcontrib><creatorcontrib>Skinner, Gabriela O</creatorcontrib><creatorcontrib>Araújo, Paulo C</creatorcontrib><creatorcontrib>Ferraz, Marcia M D</creatorcontrib><creatorcontrib>Tenório, Frank</creatorcontrib><creatorcontrib>de Almeida, Olga M M S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</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 Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>ProQuest Natural Science Collection</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 Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>PML(ProQuest Medical Library)</collection><collection>Psychology Database</collection><collection>Biological Science Database</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BMC neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Damasceno, Fabio</au><au>Skinner, Gabriela O</au><au>Araújo, Paulo C</au><au>Ferraz, Marcia M D</au><au>Tenório, Frank</au><au>de Almeida, Olga M M S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats</atitle><jtitle>BMC neuroscience</jtitle><addtitle>BMC Neurosci</addtitle><date>2013-08-30</date><risdate>2013</risdate><volume>14</volume><issue>1</issue><spage>92</spage><epage>92</epage><pages>92-92</pages><artnum>92</artnum><issn>1471-2202</issn><eissn>1471-2202</eissn><abstract>Sleep restriction alters pain perception in animals and humans, and many studies have indicated that paradoxical sleep deprivation (PSD) promotes hyperalgesia. The hyperalgesia observed after mechanical nociceptive stimulus is reversed through nitric oxide synthase (NOS) inhibition. Both nitric oxide (NO) and the dorsolateral periaqueductal gray matter (dlPAG) area of the brainstem are involved in hyperalgesia. Thus, in this work, we investigated the pain-related behavior response after mechanical noxious stimuli (electronic von Frey test), and the activity of nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), an indicator of NOS activity, within the dlPAG of paradoxical sleep-deprived rats. We also evaluated the effects of pre-treatment with L-NAME on these parameters.
These data revealed that PSD reduced the hindpaw withdrawal threshold (-47%, p < 0.0001) confirming the hyperalgesic effect of this condition. In addition, there were more NADPH-d positive cells in dlPAG after PSD than in control rats (+ 59%, p < 0.0001). L-NAME treatment prevented the reduction in the hindpaw withdrawal threshold (+ 93%, p < 0.0001) and the increase in the NADPH-d positive cells number in the dlPAG of PSD-treated rats (-36%, p < 0.0001).
These data suggest that the hyperalgesic response to mechanical noxious stimuli in paradoxical sleep-deprived rats is associated with increased NOS activity in the dlPAG, which presumably influences the descending antinociceptive pathway.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>23987566</pmid><doi>10.1186/1471-2202-14-92</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Health aspects Hyperalgesia - metabolism Kinases Male Nitric oxide Nitric Oxide - metabolism Pain Periaqueductal Gray - metabolism Physical Stimulation Rats Rats, Wistar Rodents Sleep deprivation Sleep Deprivation - metabolism |
| title | Nitric oxide modulates the hyperalgesic response to mechanical noxious stimuli in sleep-deprived rats |
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