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Stimulation of D‐2 Dopamine Receptors Decreases the Evoked In Vitro Release of [ 3 H] Acetylcholine from Rat Neostriatum: Role of K + and Ca 2+
Author(s) -
Drukarch B.,
Schepens E.,
Schoffelmeer A. N. M.,
Stoof J. C.
Publication year - 1989
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1989.tb07244.x
Subject(s) - acetylcholine , stimulation , depolarization , extracellular , chemistry , medicine , striatum , receptor , dopamine , endocrinology , acetylcholine receptor , intracellular , biophysics , biology , biochemistry
Reportedly, stimulation of D‐2 dopamine receptors inhibits the depolarization‐induced release of acetylcholine from the neostriatum in a cyclic AMP‐independent manner. In the present study, we investigated the role of K + and Ca 2+ in the D‐2 receptor‐mediated inhibition of evoked [ 3 H]acetylcholine release from rat striatal tissue slices. It is shown that the D‐2 receptor‐mediated decrease of K + ‐evoked [ 3 H]acetylcholine release is not influenced by the extracellular Ca 2+ concentration. However, increasing extracellular K + , in the presence and absence of Ca 2+ , markedly attenuates the effect of D‐2 stimulation on the K + ‐evoked [ 3 H]acetylcholine release. Furthermore, it is shown that activation of D‐2 receptors in the absence of Ca 2+ also inhibits the veratrine‐evoked release of [ 3 H]acetylcholine from rat striatum. These results suggest that the D‐2 dopamine receptor mediates the decrease of depolarization‐induced [ 3 H]acetylcholine release from rat striatum primarily by stimulation of K + efflux (opening of K + channels) and inhibition of intracellular Ca 2+ mobilization.