Amphetamine enhances latent dopaminergic neurotransmission in the rat striatum

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Abstract
The electrically evoked, calcium-dependent release of 3H-acetylcholine from slices of rat striatum was inhibited in a concentration-dependent manner by (+)-amphetamine (0.2–20 μM). This inhibitory effect of (+)-amphetamine was unaffected by depletion of the endogenous stores, of dopamine by pretreatment with rescrpine (5 mg/kg, 24h). However, the combined treatment of reserpine with α-methyl-p-tyrosine (300 mg/kg) or NSD 1015 (100 mg/kg) reduced significantly these inhibitory effects of (+)-amphetamine. Similar results were obtained after chronic 6-hydroxydopamine lesions of the corpus striatum. The inhibition of 3H-acetylcholine release by (+)-amphetamine in rats pretreated with reserpine was potentiated in the presence of 10 μM pargyline. These results support the view that the inhibitory effects of (+)-amphetamine on the electrically-evoked release of 3H-acetylcholine are mediated by dopamine released from a special pool of newly synthetized transmitter rather than through a direct action on an amphetamine recognition site or receptor.