Nitrous oxide-antinociception is mediated by opioid receptors and nitric oxide in the periaqueductal gray region of the midbrain

Emmanouil, Dimitris; Dickens, Andrea S.; Heckert, Rick W; Ohgami, Yusuke; Chung, Eunhee; Han, Shujie; Quock, Raymond M.

doi:10.1016/j.euroneuro.2007.06.008

Cited by 26 publications

(18 citation statements)

References 26 publications

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“…Other studies in the literature have shown that higher doses of nitrous oxide are also effective in producing analgesia (29)(30)(31). Some have reported that 70% nitrous oxide showed a statistically significant improvement in pain scores.…”

Section: Discussionmentioning

confidence: 94%

Effect of Nitrous Oxide on the Efficacy of the Inferior Alveolar Nerve Block in Patients with Symptomatic Irreversible Pulpitis

Stanley¹,

Drum²,

Nusstein³

et al. 2012

Journal of Endodontics

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Section: Discussionmentioning

confidence: 94%

Effect of Nitrous Oxide on the Efficacy of the Inferior Alveolar Nerve Block in Patients with Symptomatic Irreversible Pulpitis

Stanley¹,

Drum²,

Nusstein³

et al. 2012

Journal of Endodontics

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“…Antinociceptive responsiveness was assessed using the abdominal constriction test as previously described8. At varying time intervals following HBO 2 treatment, different groups of mice were treated i.p.…”

Section: Methodsmentioning

confidence: 99%

Hyperbaric Oxygen Treatment Induces a 2-Phase Antinociceptive Response of Unusually Long Duration in Mice

Chung

Zelinski

Ohgami

et al. 2010

The Journal of Pain

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Hyperbaric oxygen (HBO 2 ) therapy is approved by the FDA for limited clinical indications but is reported to produce pain relief in several chronic pain conditions. However, there have been no studies to explain this apparent analgesic effect of HBO 2 . Research conducted in our laboratory demonstrates that four daily 60-min HBO 2 treatments at 3.5 ATA induced an unparalleled antinociceptive response that consists of 1) an early phase that lasted at least six hours after the HBO 2 treatment before dissipating; and 2) a late phase that emerged about 18 hours after the early phase and lasted for up to three weeks. The early phase was sensitive to antagonism by acutely intracerebroventricular (i.c.v.)-administered opioid antagonist naltrexone and the nitric oxide synthase (NOS)-inhibitor L-NAME. The late phase was inhibited by treatment with i.c.v. naltrexone or L-NAME during the four HBO 2 treatments but was not antagonized by either naltrexone or L-NAME following acute pretreatment two weeks after HBO 2 treatment. These experimental results implicate a novel mechanism that is activated by HBO 2 , resulting in an antinociceptive response of unusually long duration that is of potential interest in the clinical management of pain.Perspective-Hyperbaric oxygen treatment of mice can induce a two-phase antinociceptive response of unusually long duration. Nitric oxide and opioid receptors appear to initiate or mediate both phases of the antinociceptive response. Further elucidation of the underlying mechanism may potentially identify molecular targets that cause long-lasting activation of endogenous analgesic systems.

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“…The underlying mechanisms of the analgesic action of N 2 O have been extensively investigated, but many aspects of the mechanism remain unclear. Since 1976 [1], there have been several reports describing the opioidergic mechanism of N 2 O-induced analgesia [2][3][4], but the opioid receptors and endogenous opioid peptides that are involved have not been clarified. We have previously shown that an absence of l-opioid receptors (MOP) in mice does not affect the analgesic effect of N 2 O or the antagonistic effect of naloxone on N 2 O-induced analgesia [5].…”

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confidence: 99%

Involvement of the κ-opioid receptor in nitrous oxide-induced analgesia in mice

Koyama

Fukuda

2010

J Anesth

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Nitrous oxide (N(2)O)-induced analgesia is thought to be mediated by endogenous opioids. We previously showed that the mu-opioid receptor is not required for the analgesic action of N(2)O in mice using a gene knockout approach. In this study, we examined the effect of kappa- (KOP)- or delta-opioid receptor (DOP)-selective antagonists on N(2)O-induced analgesia. The analgesic effect of N(2)O was evaluated using a writhing test. Male C57BL/6 mice aged 7-8 weeks were assigned to control, N(2)O, KOP agonist, and DOP agonist groups. According to the group assignment, mice were pretreated with a KOP antagonist, nor-binaltorphimine (nor-BNI), a DOP antagonist, naltrindole hydrochloride (NTI), a KOP agonist U50488, and a DOP agonist SNC80. Mice in the control, KOP agonist, and DOP agonist groups were exposed to 25% oxygen/75% nitrogen for 30 min, and mice in the N(2)O group were exposed to 25% oxygen/75% N(2)O for 30 min. Nor-BNI [10 mg kg(-1), subcutaneously (s.c.)] significantly suppressed the analgesic effect of N(2)O and U50488. In contrast, NTI (10 mg kg(-1) s.c.) did not significantly affect the analgesic action of N(2)O, but almost completely inhibited the analgesic effect of SNC80. These results suggest that KOP plays an important role in the analgesic effect of N(2)O in mice.

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Nitrous oxide-antinociception is mediated by opioid receptors and nitric oxide in the periaqueductal gray region of the midbrain

Cited by 26 publications

References 26 publications

Effect of Nitrous Oxide on the Efficacy of the Inferior Alveolar Nerve Block in Patients with Symptomatic Irreversible Pulpitis

Effect of Nitrous Oxide on the Efficacy of the Inferior Alveolar Nerve Block in Patients with Symptomatic Irreversible Pulpitis

Hyperbaric Oxygen Treatment Induces a 2-Phase Antinociceptive Response of Unusually Long Duration in Mice

Involvement of the κ-opioid receptor in nitrous oxide-induced analgesia in mice

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