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Stimulatory effect of chlordiazepoxide on locomotor activity in mice: importance of noradrenergic transmission.

Chlorodiazepoxide (CDP) produces stimulation of the locomotor activity of CD-1 and DBA/2 mice. This effect is strongly pronounced at the commencement of the testing session, and it is followed by a decline of the locomotor activity. The drugs impairing noradrenergic transmission: reserpine, clonidine and alpha-methyltyrosine, depressed or abolished the stimulatory effect of CDP; clonidine, in addition antagonized the subsequent decline of the locomotor activity in CDP-treated mice. Mice receiving reserpine subchronically (in the dose of 0.5 mg/kg daily for 3 days) displayed either motor depression or hypermotility. In approx. 50% of subchronically reserpinized mice CDP produced a strong hypermotility, lasting for at least 1 hr. It can be concluded that a noradrenergic mechanism is involved in the stimulatory effect of CDP on exploratory locomotor activity in mice, and that there exist two distinct subpopulations within the CD-1 strain, reacting differently to chronic reserpine treatment.