ABSTRACT
INTRODUCTION An amphetamine analog, /?-chloroamphetamine (PCA) has been shown to release serotonin (5-hydroxytryptamine, 5-HT) from nerve terminals, inhibit 5-HT reuptake and tryptophan hydroxylase activity, which are similar to those of the other 5-HTreleasing amphetamine analogue 3,4-methylenedioxymethamphetamine (MDMA) (Fuller, 1992; Green et al, 1995). PCA is known to deplete brain 5-HT levels for a long time by inhibiting 5-HT reuptake, and the activity of tryptophan hydroxylase, which regulates 5-HT synthesis (Fuller, 1992; Sanders-Bush et al, 1972; Steranka and Sanders-Bush, 1978). PCA induces several pharmacological effects, by facilitation of 5-HT release to the synaptic cleft. PCA stimulates secretions of several hormones such as corticosterone or prolaction (Fuller, 1992; Van de Kar, 1991). Amphetamine derivatives, including methamphetamine and MDMA, induce hyperthermic responses in rodents (Albers and Sonsalla, 1995; Green et al, 1995). We previously reported that PCA induces an apparent hyperthermia in mice similar to other amphetamine analogs and such hyperthermia is elicited by the 5-HT2A receptor (Sugimoto et al, 2000). Moreover, our previous results demonstrated that blockade of the 5-HT2B/2C receptor enhanced hyperthermic responses to PCA (Sugimoto etal, 2000).
