Does Nitrous Oxide Induce Release of Brain Opioid Peptides?

Quock, Raymond M.; Kouchich, F. J.; Tseng, Leon F.

doi:10.1097/00132586-198512000-00006

Cited by 8 publications

(8 citation statements)

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“…Exposure to 75% N 2 O for 60 minutes increased by 2-fold the amount of immunoreactive methionine-enkephalin (ME) in fractions of perfusate collected from ventricular-cisternally perfused rats. 37 At the end of N 2 O exposure, the levels of immunoreactive ME returned to baseline. This led to the conclusion that N 2 O was capable of inducing the neuronal release of either ME itself or a ME-like peptide in the rat brain.…”

Section: The Opioid Hypothesis Of N 2 O Antinociceptive Actionmentioning

confidence: 88%

Advances in Understanding the Actions of Nitrous Oxide

Emmanouil

Quock

2007

Anesthesia Progress

196

134

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Nitrous oxide (N(2)O) has been used for well over 150 years in clinical dentistry for its analgesic and anxiolytic properties. This small and simple inorganic chemical molecule has indisputable effects of analgesia, anxiolysis, and anesthesia that are of great clinical interest. Recent studies have helped to clarify the analgesic mechanisms of N(2)O, but the mechanisms involved in its anxiolytic and anesthetic actions remain less clear. Findings to date indicate that the analgesic effect of N(2)O is opioid in nature, and, like morphine, may involve a myriad of neuromodulators in the spinal cord. The anxiolytic effect of N(2)O, on the other hand, resembles that of benzodiazepines and may be initiated at selected subunits of the gamma-aminobutyric acid type A (GABA(A)) receptor. Similarly, the anesthetic effect of N(2)O may involve actions at GABA(A) receptors and possibly at N-methyl-D-aspartate receptors as well. This article reviews the latest information on the proposed modes of action for these clinical effects of N(2)O.

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Section: The Opioid Hypothesis Of N 2 O Antinociceptive Actionmentioning

confidence: 88%

Advances in Understanding the Actions of Nitrous Oxide

Emmanouil

Quock

2007

Anesthesia Progress

196

134

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“…tSignificantly different from corresponding control animals at p<0.05. and/or stimulated release of endogenous opioid peptide(s) with subsequent activation of opioid receptors (Berkowitz et al, 1979;Gillman, 1984;Quock et al, 1986;Zuniga et al, 1987a, b). …”

Section: Discussionmentioning

confidence: 99%

Influence of Chronic Ethanol Exposure on Nitrous Oxide Analgesia in Mice

1990

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The purpose of this study was to determine whether sensitivity to nitrous oxide analgesia was altered by chronic ethanol exposure. Control mice exposed to 25%, 50%, and 75% nitrous oxide in oxygen demonstrated a concentration-related analgesic effect, as measured by the acetic acid abdominal constriction test. Other mice previously exposed to ethanol vapors for 72 h exhibited a significantly reduced sensitivity to nitrous oxide analgesia. The dose-response curve of the chronic ethanol-exposed group was shifted to the right of that of the control mice. These findings suggest the possibility that subjects with a history of alcohol abuse might have reduced responsiveness to nitrous oxide in a clinical setting.

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“…In ventricularly-cisternally-perfused rats under basal urethane anesthesia, a 60-min exposure to 75% N 2 O in oxygen (O 2 ) increased methionine-enkephalin (ME)-like immunoreactivity in 8-min fractions of artificial cerebrospinal fluid (CSF) perfusate (Quock et al, 1985). In a similar study, samples of CSF were drawn from the third cerebral ventricle of dogs and fractionated to improve selectivity of the radioimmunoassay (RIA) procedure.…”

Section: Effects Of General Anesthetics On Release Of Opioid Peptidesmentioning

confidence: 99%

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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Does Nitrous Oxide Induce Release of Brain Opioid Peptides?

Cited by 8 publications

References 0 publications

Advances in Understanding the Actions of Nitrous Oxide

Advances in Understanding the Actions of Nitrous Oxide

Influence of Chronic Ethanol Exposure on Nitrous Oxide Analgesia in Mice

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

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