Abstract
Administration of single IP doses of 1.0 or 4.0 mg/kg of d-amohetamine evoked an increase in mouse spontaneous motor activity (SMA); in contrast, 1.0 mg/kg of 1-amphetamine had no significant effect, while 4.0 mg/kg caused a decreased SMA. Pretreatment with aMT or pargyline had little effect on the actions of 1-isomer, but reduced the magnitude and duration of the stimulatory effect of d-amphetamine. Pretreatment with p-chlorophenylalanine had little effect on the actions of d-amphetamine but completely abolished the depressant actions of the 1-isomer. Reserpine pretreatment markedly reduced basal SMA levels; such pretreatment caused both d- and l-amphetamine to act as stimulants of SMA.
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