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dc.contributor.authorYoshizo Matsukaen_US
dc.contributor.authorTakeshi Onoen_US
dc.contributor.authorHirotate Iwaseen_US
dc.contributor.authorSomsak Mitrirattanakulen_US
dc.contributor.authorKevin S. Omotoen_US
dc.contributor.authorTing Choen_US
dc.contributor.authorYan Yan N. Lamen_US
dc.contributor.authorBradley Snyderen_US
dc.contributor.authorIgor Spigelmanen_US
dc.contributor.otherUniversity of California, Los Angelesen_US
dc.contributor.otherOkayama Universityen_US
dc.contributor.otherJapan Ground Self Defense Force Medical Schoolen_US
dc.contributor.otherMahidol Universityen_US
dc.identifier.citationMolecular Pain. Vol.4, (2008)en_US
dc.description.abstractBackground: Adenosine 5′-triphosphate (ATP) has a ubiquitous role in metabolism and a major role in pain responses after tissue injury. We investigated the changes in basal and KCl-evoked ATP release from rat dorsal root ganglia (DRG) after peripheral neuropathy induction by unilateral sciatic nerve entrapment (SNE). Results: After SNE, rats develop long-lasting decreases in ipsilateral hindpaw withdrawal thresholds to mechanical and thermal stimulation. At 15-21 days after neuropathy induction, excised ipsilateral L4-L5 DRG display significantly elevated basal extracellular ATP levels compared to contralateral or control (naive) DRG. However, KCl-evoked ATP release is no longer observed in ipsilateral DRG. We hypothesized that the differential SNE effects on basal and evoked ATP release could result from the conversion of extracellular ATP to adenosine with subsequent activation of adenosine A1 receptors (A1Rs) on DRG neurons. Adding the selective A1R agonist, 2-chloro-N6-cyclopentyladenosine (100 nM) significantly decreased basal and evoked ATP release in DRG from naïve rats, indicating functional A1R activation. In DRG ipsilateral to SNE, adding a selective A1R antagonist, 8-cyclopentyl-1,3-dipropylxanthine (30 nM), further increased basal ATP levels and relieved the blockade of KCl-evoked ATP release suggesting that increased A1R activation attenuates evoked ATP release in neurons ipsilateral to SNE. To determine if altered ATP release was a consequence of altered DRG metabolism we compared O2consumption between control and neuropathic DRG. DRG ipsilateral to SNE consumed O2at a higher rate than control or contralateral DRG. Conclusion: These data suggest that peripheral nerve entrapment increases DRG metabolism and ATP release, which in turn is modulated by increased A1R activation. © 2008 Matsuka et al; licensee BioMed Central Ltd.en_US
dc.rightsMahidol Universityen_US
dc.subjectBiochemistry, Genetics and Molecular Biologyen_US
dc.titleAltered ATP release and metabolism in dorsal root ganglia of neuropathic ratsen_US
Appears in Collections:Scopus 2006-2010

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