okadaic-acid and 7-nitroindazole

okadaic-acid has been researched along with 7-nitroindazole* in 1 studies

Other Studies

1 other study(ies) available for okadaic-acid and 7-nitroindazole

Article	Year
The nitric oxide-cyclic GMP-protein kinase G-K+ channel pathway participates in the antiallodynic effect of spinal gabapentin. European journal of pharmacology, 2006, Feb-15, Volume: 531, Issue:1-3 The possible participation of the nitric oxide (NO)-cyclic GMP-protein kinase G (PKG) pathway on gabapentin-induced spinal antiallodynic activity was assessed in spinal nerve injured rats. Intrathecal gabapentin, diazoxide or pinacidil reduced tactile allodynia in a dose-dependent manner. Pretreatment with NG-L-nitro-arginine methyl ester (L-NAME, non-specific inhibitor of NO synthase NOS), 7-nitroindazole (neuronal NO synthase inhibitor), 1H-[1,2,4] -oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, guanylyl cyclase inhibitor) or (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), but not NG-D-nitro-arginine methyl ester (D-NAME) or okadaic acid (protein phosphatase 1 and 2 inhibitor) prevented gabapentin-induced antiallodynia. Pinacidil activity was not blocked by L-NAME, D-NAME, 7-nitroindazole, ODQ, KT-5823 or okadaic acid. Moreover, KT-5823, glibenclamide (ATP-sensitive K+ channel blocker), apamin and charybdotoxin (small- and large-conductance Ca2+-activated K+ channel blockers, respectively), but not margatoxin (voltage-gated K+ channel blocker), L-NAME, 7-nitroindazole, ODQ or okadaic acid, reduced diazoxide-induced antiallodynia. Data suggest that gabapentin-induced spinal antiallodynia could be due to activation of the NO-cyclic GMP-PKG-K+ channel pathway. Topics: Amines; Analgesics; Animals; Apamin; Carbazoles; Charybdotoxin; Cyclic GMP; Cyclic GMP-Dependent Protein Kinases; Cyclohexanecarboxylic Acids; Diazoxide; Dose-Response Relationship, Drug; Enzyme Inhibitors; Female; Gabapentin; gamma-Aminobutyric Acid; Glyburide; Indazoles; Indoles; Injections, Spinal; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Okadaic Acid; Oxadiazoles; Pain; Pinacidil; Potassium Channel Blockers; Potassium Channels; Protein Kinase Inhibitors; Quinoxalines; Rats; Rats, Wistar; Signal Transduction; Spinal Nerves; Stereoisomerism; Time Factors; Vasodilator Agents	2006

Article

Year

The nitric oxide-cyclic GMP-protein kinase G-K+ channel pathway participates in the antiallodynic effect of spinal gabapentin.

European journal of pharmacology, 2006, Feb-15, Volume: 531, Issue:1-3

The possible participation of the nitric oxide (NO)-cyclic GMP-protein kinase G (PKG) pathway on gabapentin-induced spinal antiallodynic activity was assessed in spinal nerve injured rats. Intrathecal gabapentin, diazoxide or pinacidil reduced tactile allodynia in a dose-dependent manner. Pretreatment with NG-L-nitro-arginine methyl ester (L-NAME, non-specific inhibitor of NO synthase NOS), 7-nitroindazole (neuronal NO synthase inhibitor), 1H-[1,2,4] -oxadiazolo [4,3-a] quinoxalin-1-one (ODQ, guanylyl cyclase inhibitor) or (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), but not NG-D-nitro-arginine methyl ester (D-NAME) or okadaic acid (protein phosphatase 1 and 2 inhibitor) prevented gabapentin-induced antiallodynia. Pinacidil activity was not blocked by L-NAME, D-NAME, 7-nitroindazole, ODQ, KT-5823 or okadaic acid. Moreover, KT-5823, glibenclamide (ATP-sensitive K+ channel blocker), apamin and charybdotoxin (small- and large-conductance Ca2+-activated K+ channel blockers, respectively), but not margatoxin (voltage-gated K+ channel blocker), L-NAME, 7-nitroindazole, ODQ or okadaic acid, reduced diazoxide-induced antiallodynia. Data suggest that gabapentin-induced spinal antiallodynia could be due to activation of the NO-cyclic GMP-PKG-K+ channel pathway.

Topics: Amines; Analgesics; Animals; Apamin; Carbazoles; Charybdotoxin; Cyclic GMP; Cyclic GMP-Dependent Protein Kinases; Cyclohexanecarboxylic Acids; Diazoxide; Dose-Response Relationship, Drug; Enzyme Inhibitors; Female; Gabapentin; gamma-Aminobutyric Acid; Glyburide; Indazoles; Indoles; Injections, Spinal; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase; Okadaic Acid; Oxadiazoles; Pain; Pinacidil; Potassium Channel Blockers; Potassium Channels; Protein Kinase Inhibitors; Quinoxalines; Rats; Rats, Wistar; Signal Transduction; Spinal Nerves; Stereoisomerism; Time Factors; Vasodilator Agents

2006