LOCOMOTOR EFFECTS OF NITROUS-OXIDE IN MICE - REQUIREMENT OF NEWLY-SYNTHESIZED AND MAIN INTRANEURONAL STORAGE POOLS OF DOPAMINE

Nitrous oxide increases locomotor activity in mice. Other locomotor stimulants are thought to act via central dopaminergic mechanisms and can be divided into two groups as determined by their antagonism by tyrosine hydroxylase inhibitors or by reserpine pretreatment. The purpose of the present study was to determine if nitrous oxide fits one or the other of the groups. Mice were acclimatized for 1 h to exposure chambers (4 L filtration flasks), in air, delivered at 4 L min-1 and then exposed to N2O:O2(50:50), also delivered at 4 L min-1. Locomotor activity was evaluated at 10 min intervals throughout the experiment. Racemic alpha-methyltyrosine methyl ester HCl (200 mg kg-1), administered at the beginning of acclimatization, almost totally eliminated the nitrous oxide effect but not that of methylphenidate HCl (20 mg kg-1). Reserpine pretreatment (5 mg kg-1, 18 h) totally eliminated the nitrous oxide effect but not that of amphetamine (5 mg kg-1). The results suggest that nitrous oxide requires both the newly synthesized and the main storage pools of dopamine and do not allow assignment of the agent, specifically, to either of the groups.