Dopamine inhibition of the release of endogenous acetylcholine from corpus striatum and cerebral cortex in tissue slices and synaptosomes: a presynaptic response?

The effect of dopamine on the release of endogenous acetylcholine from striatal slices and synaptosomes and from cerebral cortex synaptosomes was studied. K+ (56 mM) and veratrine (75 microM) increased the release of acetylcholine from striatal slices by 3.7 and 3.3 times the resting release, respectively. The effect of veratrine was completely abolished by tetrodotoxin (1 microM). Dopamine (10(-6) to 10(-3) M) reduced the K+-evoked release of acetylcholine from striatal slices in a dose-dependent manner. The resting release of acetylcholine was also significantly reduced by dopamine. Apomorphine (20 microM) significantly reduced the K+-evoked release of acetylcholine, and both this effect and the inhibition due to dopamine (1 mM) were significantly antagonised by chlorpromazine (20 microM). Dopamine had a similar effect on the release of acetylcholine from striatal synaptosome beds; the resting release was depressed 32% by the presence of dopamine (1 mM). A greater effect of dopamine was seen on the release of acetylcholine from cerebral cortex synaptosome beds, the resting release being reduced by 54% and the K+-evoked release by 29%. These results are discussed in terms of the possible role of presynaptic dopamine receptors in controlling the release of acetylcholine and the magnitude of their contribution compared with that of the postsynaptic dopamine receptor.