Abstract
Previously it was demonstrated that nitrous oxide antinociception in the mouse abdominal constriction test is mediated by κ-opioid receptors. Since nitrous oxide is thought to cause the neuronal release of endogenous opioid peptide to stimulate opioid receptors, this study was designed to identify the opioid peptides involved, especially in the spinal cord, by determining whether nitrous oxide antinociception can be differentially inhibited by intrathecally (i.t.) administered antisera to different opioid peptides. Male NIH Swiss mice were pretreated i.t. with rabbit antisera to opioid peptides then exposed 24 h later to one of three different concentrations of nitrous oxide in oxygen. Dose-response curves constructed from the data indicated that the antinociceptive effect of nitrous oxide was significantly antagonized by antisera to various dynorphins (DYNs) and methionine-enkephalin (ME), but not by antiserum to β-endorphin (β-EP). The AD50 values for nitrous oxide antinociception were significantly elevated by antisera to DYNs and ME but not β-EP. These findings of this study support the hypothesis that nitrous oxide antinociception in the mouse abdominal constriction test involves the neuronal release of DYN and ME in the spinal cord.
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Cahill, F.J., Ellenberger, E.A., Mueller, J.L. et al. Antagonism of nitrous oxide antinociception in mice by intrathecally administered antisera to endogenous opioid peptides. J Biomed Sci 7, 299–303 (2000). https://doi.org/10.1007/BF02253248
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DOI: https://doi.org/10.1007/BF02253248