Abstract

Nitrous oxide, like morphine, stimulates locomotor activity in the CD-1, C-57 and C-3H mouse strains. This stimulation of locomotor activity is antagonized by the narcotic antagonist naltrexone (3 and 30 mg/kg). There are several strains (A/J and DBA/2J) of mice in which morphine does not stimulate locomotor activity. Mice resistant to this behavioral effect of morphine show a stimulation of locomotor activity in response to nitrous oxide which is not blocked by naltrexone. These results provide new data linking the effects of morphine and nitrous oxide. The opiate-like stimulation of activity produced by nitrous oxide may result from the release of endogenous opiate-like substances. Nitrous oxide causes a displacement of [3H]naloxone from brain opiate receptors labeled in vivo in the CD-1 mouse strain. In marked contrast to these results, nitrous oxide administration to the A/J and DBA/2J morphine-resistant strains failed to displace [3H]naloxone from opiate receptors labeled in vivo. Thus, variations in the response to nitrous oxide may not only be strain-dependent but possibly related to deficits in the response of or interaction with the endogenous opiate system.