The acute antinociceptive effect of HBO2 is mediated by a NO–cyclic GMP–PKG–KATP channel pathway in mice

Quock, Lindsay P.; Zhang, Yao; Chung, Eunhee; Ohgami, Yusuke; Shirachi, Donald Y.; Quock, Raymond M.

doi:10.1016/j.brainres.2010.10.079

Cited by 13 publications

(18 citation statements)

References 37 publications

(42 reference statements)

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“…In earlier research, the exposure of mice to HBO 2 at 3.5 ATA has been shown to reduce the number of glacial acetic acid-induced abdominal constrictions (Zelinski et al, 2009; Ohgami et al, 2009; Chung et al, 2010; Quock et al, 2011). More recent studies in our laboratory has also demonstrated that HBO 2 treatment can provide pain relief in rats with peripheral nerve injury due to sciatic nerve crush (Gibbons et al, 2012; Gibbons et al, in press) and injections of paclitaxel (Zhang et al, 2012, 2013).…”

Section: Discussionmentioning

confidence: 94%

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Involvement of spinal cord opioid mechanisms in the acute antinociceptive effect of hyperbaric oxygen in mice

et al. 2013

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Earlier research has demonstrated that treatment with hyperbaric oxygen (HBO2) can elicit an antinociceptive response in models of acute pain. We have demonstrated that this antinociceptive effect is centrally-mediated and is dependent on opioid receptors. The purpose of the present study was to examine the role of endogenous opioid peptides and opioid receptors specifically in the spinal cord in the acute antinociceptive effect of HBO2 in mice. Male NIH Swiss mice were exposed to HBO2 (100% oxygen @ 3.5 atmospheres absolute) for 11 min and their antinociceptive responsiveness was determined using the glacial acetic acid-induced abdominal constriction test. HBO2-induced antinociception was sensitive to antagonism by intrathecal (i.t.) pretreatment with the κ- and μ-selective opioid antagonists norbinaltorphimine and β-funalrexamine, respectively, but not the δ-selective antagonist naltrindole. The antinociceptive effect of HBO2 was also significantly attenuated by i.t. pretreatment with a rabbit antiserum against rat dynorphin1-13 but not antisera against β-endorphin or methionine-enkephalin. Based on these experimental findings, the acute antinociceptive effect of HBO2 appears to involve neuronal release of dynorphin and activation of κ and μ opioid receptors in the spinal cord.

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Section: Discussionmentioning

confidence: 94%

“…I.c.v. pretreatment with the PKG-inhibitor Rp-8-(4-chlorophenylthio)-guanosine-3′,5′-cyclic monophosphorothioate interfered with the expression of the acute antinociceptive effect of HBO 2 (Quock et al, 2011). Following a 60-min/day, 4-day HBO 2 regimen, the early-phase antinociceptive effect of HBO 2 was attenuated by i.c.v.…”

Section: Discussionmentioning

confidence: 99%

Involvement of spinal cord opioid mechanisms in the acute antinociceptive effect of hyperbaric oxygen in mice

et al. 2013

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“…Mice treated with an i.p. injection of glacial acetic acid then placed into a hyperbaric chamber exhibited a reduced number of abdominal constrictions during a 6-min observation period under HBO 2 at 3.5 ATA (Ohgami et al, 2009; Quock et al, 2011). …”

Section: Discussionmentioning

confidence: 99%

“…Research from our laboratory demonstrated that HBO 2 treatment effectively reduces pain in animal models of acute pain (Ohgami et al, 2009; Zelinski et al, 2009a; Chung et al, 2010; Quock et al, 2011). Our results from these experiments show that HBO 2 -induced antinociception is significantly attenuated by the opioid antagonist naltrexone (NTX).…”

Section: Introductionmentioning

confidence: 99%

Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain

et al. 2013

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Earlier research has demonstrated that hyperbaric oxygen (HBO2) can produce an antinociceptive effect in models of acute pain. Recent studies have revealed that HBO2 can produce pain relief in animal models of chronic pain as well. The purpose of the present investigation was to ascertain whether HBO2 treatment might suppress allodynia in rats with neuropathic pain and whether this effect might be blocked by the opioid antagonist naltrexone (NTX). Male Sprague Dawley rats were subjected to a sciatic nerve crush under anesthesia and mechanical thresholds were assessed using an electronic von Frey anesthesiometer. The time course of the HBO2-induced anti-allodynic effect in different treatment groups was plotted, and the area-under-the-curve (AUC) was determined for each group. Seven days after the nerve crush procedure, rats were treated with HBO2 at 3.5 atmospheres absolute (ATA) for 60 min and exhibited an anti-allodynic effect, compared to nerve crush-only control rats. Twenty-four hours before HBO2 treatment, another group of rats was implanted with Alzet® osmotic minipumps that continuously released NTX into the lateral cerebral ventricle for 7 days. These NTX-infused, HBO2-treated rats exhibited an allodynic response comparable to that exhibited by rats receiving nerve crush only. Analysis of the AUC data showed that HBO2 significantly reduced the nerve crush-induced allodynia; this anti-allodynic effect of HBO2 was reversed by NTX. These results implicate opioid receptors in the pain relief induced by HBO2.

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“…L-NMMA and carboxy-PTIO was dissolved in bacteriostatic saline. Based on previous experiments in our laboratory (McDonald et al 1994; Quock et al 2011), the dose of L-NMMA was 10 mg/kg, the dose of carboxy-PTIO was 0.6 mg/kg, the dose of ODQ was 0.01 mg/kg, and the dose of flumazenil was 10 mg/kg. The effect of pretreatment drugs alone on time spend in the light compartment of the light/dark box is shown in Fig.…”

Section: Methodsmentioning

confidence: 99%

An anxiolytic-like effect of hyperbaric oxygen in the mouse light/dark exploration test

2012

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Aims We studied whether hyperbaric oxygen (HBO2) treatment, which is known to increase production of nitric oxide (NO) in the brain, might also produce an NO-dependent anxiolytic-like behavioral response. Main methods Male NIH Swiss mice (20–25 g) were subjected to a 60-min HBO2 treatment at different absolute atmospheres, and anxiety was assessed using the light/dark exploration test at different time intervals following the cessation of HBO2 treatment. To ascertain the underlying mechanism of action, other groups of mice were pretreated with the NO synthase inhibitor NG-monomethyl-L-arginine acetate, the NO scavenger 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3-oxide (carboxy-PTIO), the soluble guanylyl cyclase-inhibitor 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ) or the benzodiazepine antagonist flumazenil to determine their influence on the HBO2-induced anxiolytic-like effect. Key findings A 60-min HBO2 treatment at 3.0 absolute atmospheres increased the time spent by mice in the light compartment that lasted up to 90 min following the end of HBO2 treatment. This anxiolytic effect of HBO2 was significantly reduced by pretreatment with L-NMMA, carboxy-PTIO, ODQ and flumazenil. Significance Based on these findings, we conclude that a 60-min HBO2 treatment is capable of inducing an anxiolytic effect that possibly involves NO, cyclic GMP and the benzodiazepine binding site.

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The acute antinociceptive effect of HBO2 is mediated by a NO–cyclic GMP–PKG–KATP channel pathway in mice

Cited by 13 publications

References 37 publications

Involvement of spinal cord opioid mechanisms in the acute antinociceptive effect of hyperbaric oxygen in mice

Involvement of spinal cord opioid mechanisms in the acute antinociceptive effect of hyperbaric oxygen in mice

Involvement of brain opioid receptors in the anti-allodynic effect of hyperbaric oxygen in rats with sciatic nerve crush-induced neuropathic pain

An anxiolytic-like effect of hyperbaric oxygen in the mouse light/dark exploration test

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