The potent inducible nitric oxide synthase inhibitor ONO-1714 inhibits neuronal NOS and exerts antinociception in rats

Sekiguchi, Fumiko; Mita, Yoko; Kamanaka, Yoshihisa; Kawao, Naoyuki; Matsuya, Hidekazu; Taga, Chiyomi; Kawabata, Atsufumi

doi:10.1016/j.neulet.2004.04.069

Cited by 19 publications

(13 citation statements)

References 24 publications

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“…However, the role played by spinal iNOS during peripheral inflammation is controversial (Dolan et al, 2000;Tao et al, 2003;Sekiguchi et al, 2004). Our result clearly indicates that iNOS increases about 3-fold versus control 6 h following carrageenan administration.…”

Section: Discussionmentioning

confidence: 70%

Acute Intracerebroventricular Administration of Palmitoylethanolamide, an Endogenous Peroxisome Proliferator-Activated Receptor-α Agonist, Modulates Carrageenan-Induced Paw Edema in Mice

D’Agostino¹,

Rana²,

Russo³

et al. 2007

J Pharmacol Exp Ther

133

109

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Section: Discussionmentioning

confidence: 70%

Acute Intracerebroventricular Administration of Palmitoylethanolamide, an Endogenous Peroxisome Proliferator-Activated Receptor-α Agonist, Modulates Carrageenan-Induced Paw Edema in Mice

D’Agostino¹,

Rana²,

Russo³

et al. 2007

J Pharmacol Exp Ther

133

109

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“…Doses of L-NAME, that were ineffective in our model, were significantly higher than those used to block pain enhancement due to intrathecal fractalkine (Milligan et al, 2005) and equivalent to those used to block phase 2 formalin responses (Malmberg and Yaksh, 1993c). Although higher doses of intrathecal L-NAME (above 150 μg) are required to reverse thermal hyperalgesia induced by carrageenan (Osborne and Coderre, 1999;Sekiguchi et al, 2004), this model has both NMDA and Ca 2+ permeable AMPA/kainite receptor components (Sorkin et al, 2001). Importantly, intrathecal administration of the same dose that we employed (30 μg) was shown to inhibit local spinal nitric oxide synthase by more than 80% (Salter et al, 1996).…”

Section: Discussionmentioning

confidence: 87%

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Sorkin

Doom

Maruyama

et al. 2008

European Journal of Pharmacology

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Various animal models of pain are dependent on activation of different glutamate receptor subtypes. First-degree burn of the paw elicits a secondary hyperalgesia that is dependent on Ca 2++ permeable α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), but not N-methyl-D-aspartate (NMDA) receptors. The present study takes advantage of that specificity by examining the effects of spinal pretreatments of agents on this secondary hyperalgesia. Rats with indwelling intrathecal catheters were pretreated with agents prior to paw injury. Mechanical withdrawal thresholds were measured before, and for three h after the injury.Spinal pretreatment with cyclooxygenase (10 and 30 μg (S)-(+)-ibuprofen; and 3 and 30 μg ketorolac) and nitric oxide synthase (33 and 100 μg N G Nitro-L-arginine methyl ester hydrochloride (L-NAME) and 10 μg thiocitrulline) inhibitors resulted in no specific anti-allodynia. In contrast, ziconotide (0.3, 1.0 and 3 μg), the N-type voltage gated calcium channel antagonist was very effective in blocking burn-induced sensitivity at all doses used. L-type (Diltiazam 230 μg) and P-type (Agatoxin IVA 0.3 μg) calcium channel blockers produced intermediate effects. Thus, cyclooxygenase and nitric oxide synthase are assumed not to be downstream of Ca 2++ permeable AMPA receptors. Voltage gated calcium channels blockers could exert their effects either pre-or post-synaptically.

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“…Benzyl substitution at the 6-position (36) gives the most selectivity for human nNOS (IC 50 = 0.9 µM) over eNOS (IC 50 = 44 µM) and iNOS (IC 50 = 9.2 µM) [95]. (1S, 5S, 6R, 7R)-7-Chloro-3-imino-5-methyl-2-azabicyclo[4.1.0] heptane hydrochloride (37, ONO-1714) is an iNOS inhibitor that was found to have nNOS inhibitory potency in vitro but not in vivo, presumably because of its poor blood-brain barrier permeability [96,97].…”

Section: -Iminopiperidinesmentioning

confidence: 99%

Selective Neuronal Nitric Oxide Synthase Inhibitors

Erdal¹,

Litzinger²,

Seo³

et al. 2005

CTMC

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This review includes the non-patent literature up to October 2004 that deals with selective neuronal nitric oxide synthase inhibitors (highest potency is for the neuronal isozyme). Some non-selective inhibitors or selective inducible nitric oxide synthase inhibitors are mentioned if they are related to compounds that are discussed; structures of these compounds generally are not given. In vitro inhibition constants are given either as IC(50) values or as K(i)values. An IC(50) value, the inhibitor concentration that produces 50% inhibition in the presence of a constant concentration of substrate, is obtained by extrapolation of several rate data points to 50% inhibition. K(i) values are derived from several types of plots that relate the concentration of inhibitor with enzyme velocity in the presence of a variety of substrate concentrations [1]. The K(i) value can be estimated from the IC(50) value [2]. Although the two inhibition constants are related, they are not the same; generally, the reported K(i) values tend to be lower than the IC(50) values. If specifics are desired about how the data were collected, then the reader will have to look in the literature cited. No attempt was made to be exhaustive in citing all references related to specific inhibitors; rather, examples of literature references are given for each inhibitor described.

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The potent inducible nitric oxide synthase inhibitor ONO-1714 inhibits neuronal NOS and exerts antinociception in rats

Cited by 19 publications

References 24 publications

Acute Intracerebroventricular Administration of Palmitoylethanolamide, an Endogenous Peroxisome Proliferator-Activated Receptor-α Agonist, Modulates Carrageenan-Induced Paw Edema in Mice

Acute Intracerebroventricular Administration of Palmitoylethanolamide, an Endogenous Peroxisome Proliferator-Activated Receptor-α Agonist, Modulates Carrageenan-Induced Paw Edema in Mice

Secondary hyperalgesia in the rat first degree burn model is independent of spinal cyclooxygenase and nitric oxide synthase

Selective Neuronal Nitric Oxide Synthase Inhibitors

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