Abstract
We have previously shown that the antinociceptive effect of nitrous oxide (N 2O) in the rat hot plate test is sensitive to antagonism by antisera against the endogenous opioid peptide β-endorphin. Moreover, N 2O-induced antinociception is reduced by inhibition of nitric oxide (NO) production in the brain. To test the hypothesis that N 2O might stimulate an NO-dependent neuronal release of β-endorphin, we conducted a ventricular-cisternal perfusion with artificial cerebrospinal fluid (aCSF) in urethane-anesthetized Sprague–Dawley rats. Ten-minute fractions of aCSF perfusate were collected from separate groups of room air-exposed rats, N 2O-exposed rats, and L-NAME-pretreated, N 2O-exposed rats; they were then analyzed for their content of NO metabolites and β-endorphin. Compared to room air control, exposure to 70% N 2O increased perfusate levels of the NO metabolites nitrite and nitrate as well as β-endorphin. Pretreatment of rats with L-N G-nitro arginine methyl ester, an inhibitor of NO synthase, prevented the N 2O-induced increases in nitrite, nitrate and β-endorphin. These findings demonstrate in an in vivo rat model that N 2O may stimulate an NO-dependent neuronal release of β-endorphin.
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
