Dopamine Inhibition of the Release of Endogenous Acetylcholine from Corpus Striatum and Cerebral Cortex in Tissue Slices and Synaptosomes: A Presynaptic Response?

Abstract

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.

Serotonergic modulation of dopamine measured with [11C]raclopride and PET in normal human subjects

“…Subsequent studies in the adult baboon and in human subjects demonstrated that PET could be used to measure the modulation of dopamine by the primary neurotransmitters known to modulate its activity (e.g., γ-aminobutyric acid, acetylcholine, serotonin) (14)(15)(16). These results were remarkably consistent with the basic neuroanatomic and neurophysiologic data concerning the modulation of dopamine in the rat and nonhuman primate brain (17)(18)(19).…”

Ultrastructural immunocytochemical localization of neurotensin and the dopamine D2 receptor in the rat nucleus accumbens

“…Based upon the formation of symmetric junctions by these terminals which contained D2-LI, DA is likely to modulate the presynaptic release of an inhibitory neurotransmitter (Cohen et al, 1982) such as GABA (Beart et al, 1979) or acetylcholine (DeBelleroche et al, 1982;Chesselet, 1984). Thus, in addition to having direct effects on NTreceptive neurons, DA may also indirectly stimulate (i.e., "disinhibit") neurons which are responsive to NT.…”

“…Accordingly, the Dz-immunolabeled organelles in aspiny neurons may reflect insertion of the Dz receptor into membranes en route to or from axon terminals. Stimulation of D2 heteroreceptors on axon terminals is known to inhibit the release of a variety of neurotransmitters, including acetylcholine (DeBelleroche et al, 1982;Chesselet, 1984). Furthermore, cholinergic neurons of the striatum have recently been shown to express mRNA for the D2 receptor (MacLennan et al, 1994).…”

Inhibition of cortical acetylcholine release and cognitive performance by histamine H3 receptor activation in rats

“…Hence, the inhibition is likely to be indirect, mediated by the release of another transmitter(s) which, in turn, inhibits ACh release. Substances present in the cortex and inhibiting ACh release are noradrenaline (Beani et al, 1978), dopamine (De Belleroche et al, 1982) and adenosine (Vizi & Knoll, 1976). The potential candidate is probably released by cortical interneurones.…”