کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2534804 | 1559100 | 2008 | 7 صفحه PDF | دانلود رایگان |

The possible participation of the nitric oxide (NO)-cyclic GMP-protein kinase G (PKG)-K+ channel pathway on melatonin-induced local antinociception was assessed during the second phase of the formalin test. The local peripheral ipsilateral, but not contralateral, administration of melatonin (150—600 μg/paw) produced a dose-related antinociception during both phases of the formalin test in rats. Moreover, local pretreatment with NG-l-nitro-arginine methyl ester (l-NAME, NO synthesis inhibitor, 10–100 μg/paw), 1H-(1,2,4)-oxadiazolo(4,2-a)quinoxalin-1-one (ODQ, guanylyl cyclase inhibitor, 5–50 μg/paw), (9S, 10R, 12R)-2,3,9,10,11,12-hexahydro-10-methoxy-2,9-dimethyl-1-oxo-9,12-epoxy-1H-diindolo [1,2,3-fg:3′,2′,1′-kl]pyrrolo [3,4-i][1,6] benzodiazocine-10-carboxylic acid methyl ester (KT-5823, specific PKG inhibitor, 50–500 ng/paw), glibenclamide (ATP-sensitive K+ channel blocker, 5–50 μg/paw), apamin (small-conductance Ca2+-activated K+ channel blocker, 0.1–1 μg/paw) or charybdotoxin (large- and intermediate-conductance Ca2+-activated K+ channel blocker, 0.03–0.3 μg/paw), but not NG-d-nitro-arginine methyl ester (d-NAME, inactive isomer of l-NAME, 100 μg/paw) or vehicle, significantly prevented melatonin (300 μg/paw)-induced antinociception. Data suggest that melatonin-induced local peripheral antinociception during the second phase of the test could be due to activation of the NO-cyclic GMP-PKG-ATP-sensitive and Ca2+-activated K+ channels pathway.
Journal: European Journal of Pharmacology - Volume 596, Issues 1–3, 31 October 2008, Pages 70–76