Role of Brain Dynorphin in Nitrous Oxide Antinociception in Mice

Branda, Emily M; Ramza, Justin T.; Cahill, Francis J.; Tseng, Leon F.; Quock, Raymond M.

doi:10.1016/s0091-3057(99)00202-6

Cited by 37 publications

(30 citation statements)

References 23 publications

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“…Since we have proposed in earlier investigations that N 2 O owes its antinociceptive effect in animals to stimulated neuronal release of endogenous opioid peptides (Branda et al, 2000;Cahill et al, 2000), the importance of the present findings is the localization of both opioid and NO mechanisms in the PAG of the midbrain. In as much as inhibition of NOS can significantly attenuate the increase in release of methionine-enkephalin in the rat spinal cord in response to centrally-administered β-endorphin (Hara et al, 1995), one explanation of these findings is that NO may play a key regulatory role in the N 2 O-stimulated neuronal release of endogenous opioid peptides that then activate opioid receptors in the PAG.…”

Section: Discussionsupporting

confidence: 51%

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

Emmanouil

Dickens

Heckert

et al. 2008

European Neuropsychopharmacology

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Previous studies have shown that nitrous oxide (N 2 O)-induced antinociception is sensitive to antagonism by blockade of opioid receptors and also by inhibition of nitric oxide (NO) production. The present study was conducted to determine whether these occur within the same brain site. Mice were stereotaxically implanted with microinjection cannulae in the periaqueductal gray (PAG) area of the midbrain. In saline-pretreated mice, exposure to 70% N 2 O resulted in a concentrationdependent antinociceptive effect in the mouse abdominal constriction test. Pretreatment with an opioid antagonist in the PAG significantly antagonized the antinociceptive effect. Pretreatment with an inhibitor of NO production in the PAG also significantly antagonized the antinociceptive effect. These findings suggest that N 2 O acts in the PAG via an NO-dependent, opioid receptor-mediated mechanism to induce antinociception.

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Section: Discussionsupporting

confidence: 51%

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

Emmanouil

Dickens

Heckert

et al. 2008

European Neuropsychopharmacology

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“…The depression in dopamine levels may be associated with compensatory increases in striatal dynorphinergic activity (Steiner & Gerfen, 1998), given the role that dynorphin opioid peptides play in N 2 O-mediated antinociception especially at low doses before higher order anesthetic mechanisms are induced (Branda et al 2000). Collectively, these studies support the hypothesis that exposure to N 2 O may affect memory formation in a time and exposure-dependent manner.…”

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confidence: 54%

Letter to the Editor: Exposure to nitrous oxide and intrusive memory formation in psychological trauma

Fluegge¹

2017

Psychol. Med.

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“…N 2 O must, therefore, activate a mechanism or cascade that continues to its ultimate conclusion (antinociception) despite termination of exposure and the rapid elimination of N 2 O from the body in the expired air. That central mechanism is hypothesized to be the stimulated neuronal release of dynorphin with subsequent activation of central -opioid receptors (Branda et al, 2000;Cahill et al, 2000). The N 2 O-induced antinociceptive effect was dose dependently antagonized by SMTC and L-NIO but not AMT.…”

Section: Nos In N 2 O Antinociception In Mice 487mentioning

confidence: 99%

“…and i.t. pretreatment with rabbit antisera against rat dynorphin (Branda et al, 2000;Cahill et al, 2000).…”

mentioning

confidence: 99%

Role of Nitric-Oxide Synthase Isoforms in Nitrous Oxide Antinociception in Mice

Ishikawa

Quock²

2003

J Pharmacol Exp Ther

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Exposure of mice to the anesthetic gas N 2 O evokes a prominent antinociceptive effect that is sensitive to antagonism by nonselective nitric-oxide synthase (NOS) inhibitors. The present study was conducted to identify whether a specific NOS isoform is implicated in N 2 O antinociception in mice. In the abdominal constriction test, exposure of mice to 25, 50, and 70% N 2 O resulted in a concentration-dependent antinociceptive effect that persisted for up to 6 min following removal of the mice from the N 2 O atmosphere into room air. This N 2 O antinociceptive effect was antagonized by pretreatment with S-methyl-Lthiocitrulline (SMTC) and higher doses of L-N 5 -(1-iminoethyl)-ornithine (L-NIO), which reportedly inhibit the neuronal and endothelial isoforms of NOS, respectively. Nevertheless, the N 2 O-induced antinociception was unaffected by pretreatment with low doses of either SMTC or L-NIO or by pretreatment with 2-amino-5,6-dihydro-6-methyl-4H-1,3-thiazine (AMT), which selectively inhibits inducible NOS. The s.c. pretreatment with SMTC and L-NIO reduced brain NOS activity in a dose-dependent manner, whereas AMT had no such effect. Moreover, in blood pressure experiments, SMTC increased SBP in doseunrelated fashion, whereas L-NIO showed an appreciably weaker but dose-related increase in SBP. The i.c.v. pretreatment with SMTC also reduced N 2 O antinociception and brain NOS activity without increasing of SBP. These results suggest that it is the neuronal isoform of NOS that is involved in mediation of the antinociceptive effect of N 2 O in the mice.

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Role of Brain Dynorphin in Nitrous Oxide Antinociception in Mice

Cited by 37 publications

References 23 publications

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

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

Letter to the Editor: Exposure to nitrous oxide and intrusive memory formation in psychological trauma

Role of Nitric-Oxide Synthase Isoforms in Nitrous Oxide Antinociception in Mice

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