Neurobiology of nitrous oxide-induced antinociceptive effects
by
Fujinaga M, Maze M.
Magill Department of Anaesthesia,
Intensive Care and Pain Management Chelsea
and Westminster Hospital, London, UK.
m.fujinaga@ic.ac.uk
Mol Neurobiol. 2002 Apr;25(2):167-89

ABSTRACT

Nitrous oxide (N2O), or laughing gas, has been used for clinical anesthesia for more than a century and is still commonly used. While the anesthetic/hypnotic mechanisms of N2O remain largely unknown, the underlying mechanisms of its analgesic/antinociceptive effects have been elucidated during the last several decades. Evidence to date indicate that N2O induces opioid peptide release in the periaqueductal gray area of the midbrain leading to the activation of the descending inhibitory pathways, which results in modulation of the pain/nociceptive processing in the spinal cord. The types of opioid peptide induced by N2O and the subtypes of opioid receptors that mediate the antinociceptive effects of N2O appear to depend on various factors including the species and/or strain, the regions of the brain, and the paradigms of behavior testing used for the experiments. Among three types of descending inhibitory pathways, the descending noradrenergic inhibitory pathway seems to play the most prominent role. The specific elements involved are now being resolved.

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Inhaled anaesthetics
Rats on nitrous oxide
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200 years of laughing gas
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Nitrous oxide: 'laughing gas'
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Beta-endorphin/nitrous oxide withdrawal
Nitrous oxide - subjective and rewarding effects
Whipped cream bulbs cause nitrous oxide myelopathy

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