Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides

Cahill, Francis J.; Ellenberger, Elizabeth A.; Mueller, Janet L.; Tseng, Leon F.; Quock, Raymond M.

doi:10.1007/bf02253248

Cited by 25 publications

(12 citation statements)

References 15 publications

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“…Once again, this is similar to observations made in studies of N 2 O-induced antinociception. Supraspinal pretreatment of mice with DYN AS significantly antagonized the antinociceptive of N 2 O, while β-EP AS and ME AS were without effect1,2.…”

Section: Discussionmentioning

confidence: 91%

A Prolonged Nitric Oxide-Dependent, Opioid-Mediated Antinociceptive Effect of Hyperbaric Oxygen in Mice

Zelinski

Ohgami

Chung

et al. 2009

The Journal of Pain

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Hyperbaric oxygen (HBO 2 ) therapy is reported to cause pain relief in several conditions of chronic pain. A single 60-min session of HBO 2 treatment produced a prolonged antinociceptive effect in mice that persisted for 90 min after cessation of treatment. The HBO 2 -induced antinociception was significantly attenuated by pretreatment prior to HBO 2 exposure with the opioid antagonist naltrexone, the non-specific nitric oxide synthase (NOS)-inhibitor N G -nitro-L-arginine methyl ester (L-NAME) and the selective neuronal NOS-inhibitor S-methyl-L-thiocitrulline (SMTC) but not the selective endothelial NOS-inhibitorThe antinociception was also significantly reduced by central pretreatment with a rabbit antiserum against dynorphin 1-13 but not by rabbit antisera against either β-endorphin or methionine-enkephalin. The prolonged antinociceptive effect at 90 min after HBO 2 -induced treatment was also significantly attenuated by naltrexone but not L-NAME administered 60 min following HBO 2 treatment but prior to nociceptive testing. These findings indicate that the antinociception that persists for 90 min after HBO 2 exposure is mediated by nitric oxide (NO) and opioid mechanisms but that the NO involvement is critical during the HBO 2 treatment and not at the time of nociceptive testing. These results are consistent with the concept that HBO 2 may induce an NO-dependent release of opioid peptide to cause a long-acting antinociceptive effect. Words for IndexingHyperbaric Oxygen; Nitric Oxide; Opioid; Antinociception; Mice Corresponding Author: Dr. Raymond M. Quock, Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, P.O. Box 646534, Pullman,. Perspective This article present evidence of a persistent antinociceptive effect of hyperbaric oxygen treatment that is mediated by opioid and nitric oxide mechanisms. Further elucidation of the underlying mechanism could potentially identify molecular targets to cause a longer-acting activation of endogenous pain-modulating systems.

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Section: Discussionmentioning

confidence: 91%

A Prolonged Nitric Oxide-Dependent, Opioid-Mediated Antinociceptive Effect of Hyperbaric Oxygen in Mice

Zelinski

Ohgami

Chung

et al. 2009

The Journal of Pain

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“…or intrathecal (i.t.) pretreatment with antisera against various dynorphin fragments but not antisera against ME or h-endorphin (Branda et al, 2000;Cahill et al, 2000). The suggested neuronal release of dynorphin in the mouse was supported by the finding that N 2 O-induced antinociception was selectively and significantly enhanced by i.c.v.…”

Section: An Opioid Component To General Anesthesia?mentioning

confidence: 65%

Do inhalation general anesthetic drugs induce the neuronal release of endogenous opioid peptides?

Quock

Vaughn

2005

Life Sciences

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The antagonism of some effects of inhalation general anesthetic agents by naloxone suggests that there may be an opioid component to anesthetic action. There is evidence that this opioid action component is due to neuronal release of endogenous opioid peptides. The strongest evidence is provided by studies that monitor changes in the concentration of opioid peptides in the perfused brain following inhalation of the anesthetic. Indirect or circumstantial evidence also comes from studies of anesthetic effects on regional brain levels of opioid peptides, antagonism of selected anesthetic effects by antisera to opioid peptides and anesthetic-induced changes radioligand binding to opioid receptors. It is likely that some inhalation general anesthetics (e.g., nitrous oxide) can induce neuronal release of opioid peptides and that this may contribute to certain components of general anesthesia (e.g., analgesia). More definitive studies utilizing in vivo microdialysis or autoradiography in selected areas of the brain during induction and successive states of general anesthesia have yet to be conducted.

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“…and i.t. pretreatment with the selective κ opioid antagonist norbinal-torphimine (Quock et al, 1990) and rabbit antiserum against rat dynorphin (Branda et al, 2000; Cahill et al, 2000). How is this reconciled with the present findings that implicate an NO–cyclic GMP–PKG pathway in the antinociceptive activity of N 2 O?…”

Section: Discussionmentioning

confidence: 99%

Involvement of a NO–cyclic GMP–PKG signaling pathway in nitrous oxide-induced antinociception in mice

Zhang

Quock

Chung

et al. 2011

European Journal of Pharmacology

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The antinociceptive effect of nitrous oxide (N2O) is dependent on nitric oxide (NO); however, the next step in the pathway activated by NO is undetermined. The present study was conducted to test the hypothesis that a N2O action involves sequential activation of NO synthase, soluble guanylyl cyclase and protein kinase G to induced an antinociceptive effect in mice. The antinociceptive responsiveness of male NIH Swiss mice to N2O was assessed using the acetic acid abdominal constriction test. Different groups of mice were pretreated with either saline, the NO scavenger 2-(4-carboxyphenyl)-4,5-dihydro-4,4,5,5-tetramethyl-1H-imidazolyl-1-oxy-3-oxide (carboxy-PTIO), the guanylyl cyclase-inhibitor (1H-[1,2,4]-oxadiazolo-[4,3-a]quinoxalin-1-one) (ODQ), the protein kinase G-inhibitor Rp-isomer of 8-(4-chlorophenylthio)-guanosine-3',5'-cyclic monophosphorothioate (Rp-8-pCPT-cGMPS) or the selective phosphodiesterase V-inhibitor 1,2-dihydro-2-[(2-methyl-4-pyridinyl)methyl]-1-oxo-8-(2-pyrimidinylmethoxy)-4-(3,4,5-trimethoxyphenyl)-2,7-naphthyridine-3-carboxylic acid methyl ester hydrochloride (T 0156). Vehicle (saline)-pretreated mice responded to N2O in a concentration-dependent manner. This antinociceptive effect was antagonized by systemic pretreatment with carboxy-PTIO and ODQ and central pretreatment with Rp-8-pCPT-cGMPS. In each case, the dose-response curve for N2O was progressively shifted to the right by increasing doses of each pretreatment drug. On the other hand, N2O-induced antinociception was enhanced by systemic pretreatment with T 0156; the dose-response curve for N2O was shifted to the left. The ATP-sensitive potassium channel blocker glibenclamide was without influence on the anti-nociceptive effect of N2O. These results support the hypothesis that N2O-induced antinociception in mice is mediated by a NO–cyclic GMP–PKG pathway.

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Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides

Cited by 25 publications

References 15 publications

A Prolonged Nitric Oxide-Dependent, Opioid-Mediated Antinociceptive Effect of Hyperbaric Oxygen in Mice

A Prolonged Nitric Oxide-Dependent, Opioid-Mediated Antinociceptive Effect of Hyperbaric Oxygen in Mice

Do inhalation general anesthetic drugs induce the neuronal release of endogenous opioid peptides?

Involvement of a NO–cyclic GMP–PKG signaling pathway in nitrous oxide-induced antinociception in mice

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