β-Phenylethylamine modulates acetylcholine release in the rat striatum:: involvement of a dopamine D2 receptor mechanism

We examined the effects of beta -phenylethylamine on striatal acetylcholine release in freely moving rats using in vivo microdialysis. beta -Phenylethylamine at 12.5 mg/kg, i.p. did not affect acetylcholine release in the striatum, whereas 25 and 50 mg/kg, i.p. immediately induced an increase in acetylcholine release in the striatum at 15-45 min. This increase following intraperitoneal administration of beta -phenylethylamine (25 mg/kg) was not affected by locally applied SCH-23390(R(+)-7-chloro-8-hydroxy-3-methyl-1-phenyl-2,3,4,5-tetrahydro-1 H-3-benzazepine, 10 muM), a dopamine D-1 receptor antagonist, nor by raclopride (10 muM), a dopamine D-2 receptor antagonist. The increased release of acetylcholine induced by beta -phenylethylamine was suppressed by local infusion of tetrodotoxin (1 muM). In contrast, the extracellular acetylcholine level in the striatum was significantly decreased by local application of beta -phenylethylamine (10 and LOO muM) in the striatum via a microdialysis probe. The decrease was completely blocked by local co-application of raclopride (10 muM) The beta -phenylethylamine-induced decrease in striatal acetylcholine release was not affected by co-perfusion with SCH-23390 (10 muM). These results indicate that systemic administration of beta -phenylethylamine increases acetylcholine release, whereas locally applied beta -phenylethylamine decreases striatal acetylcholine release in freely moving rats. Furthermore, the dopaminergic system, through the dopamine D-2 receptor, is involved in the locally applied beta -phenylethylamine-induced decrease in acetylcholine in the striatum. (C) 2001 Elsevier Science B.V., All rights reserved.