Activation of dopamine D1 receptors does not affect D2 receptor-mediated inhibition of acetylcholine release in rabbit striatum
Language English Country Germany Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
1347152
DOI
10.1007/bf00175463
Knihovny.cz E-resources
- MeSH
- Acetylcholine metabolism MeSH
- Corpus Striatum drug effects metabolism MeSH
- Dopamine pharmacology MeSH
- Dopamine Agents pharmacology MeSH
- Electric Stimulation MeSH
- Electrophysiology MeSH
- Rabbits MeSH
- Receptors, Dopamine physiology MeSH
- Receptors, Dopamine D1 MeSH
- Receptors, Dopamine D2 MeSH
- Animals MeSH
- Check Tag
- Rabbits MeSH
- Male MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylcholine MeSH
- Dopamine MeSH
- Dopamine Agents MeSH
- Receptors, Dopamine MeSH
- Receptors, Dopamine D1 MeSH
- Receptors, Dopamine D2 MeSH
The possible involvement of dopamine D1 receptors in the regulation of acetylcholine release in the rabbit caudate nucleus was investigated. Caudate slices, preincubated with [3H]choline, were superfused continuously and subjected to electrical field stimulation with only a single pulse. In agreement with the view that the release of acetylcholine evoked by a single electrical pulse is not influenced by endogenous transmitters, atropine and domperidone failed to increase the evoked release of [3H]acetylcholine, whereas oxotremorine and quinpirole caused a concentration-dependent inhibition of transmitter release. Neither the dopamine D1 receptor antagonist SCH 23390 nor the D1 agonist SKF 38393 in a concentration range of 0.01-1 mumol/l changed the evoked [3H]acetylcholine release. The inhibitory effect of the dopamine D2 receptor agonist quinpirole was virtually abolished in the presence of 0.1 mumol/l domperidone and diminished in the presence of 1 mumol/l SCH 23390. It remained unchanged in the presence of 1 mumol/l SKF 38393. It is concluded that the inhibition of acetylcholine release by dopamine is mediated exclusively via presynaptic dopamine D2 receptors and that the antagonistic effect of SCH 23390 on the inhibition of acetylcholine release by quinpirole is due to its interaction with dopamine D2 rather than D1 receptors located on cholinergic nerve terminals.
See more in PubMed
Brain Res. 1982 Nov 4;250(2):263-70 PubMed
Neuroscience. 1990;37(1):1-9 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1983 Aug;323(4):298-306 PubMed
Eur J Pharmacol. 1984 Oct 1;105(1-2):73-83 PubMed
Eur J Pharmacol. 1990 Sep 21;186(2-3):335-8 PubMed
Life Sci. 1986 Jun 16;38(24):2247-54 PubMed
Brain Res. 1977 Jun 10;128(2):285-91 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1984 Sep;327(2):180-2 PubMed
Brain Res. 1990 Jun 4;518(1-2):193-8 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1980;315(2):111-7 PubMed
Brain Res. 1977 Mar 11;123(2):311-22 PubMed
Trends Pharmacol Sci. 1988 Aug;9(8):274-6 PubMed
J Neurochem. 1983 Jul;41(1):94-101 PubMed
Life Sci. 1982 Dec 20;31(25):2883-90 PubMed
J Pharmacol Exp Ther. 1987 Jul;242(1):300-5 PubMed
Naunyn Schmiedebergs Arch Pharmacol. 1988 Dec;338(6):632-43 PubMed
Br J Pharmacol. 1974 Dec;52(4):499-507 PubMed
J Neurochem. 1990 Jun;54(6):2145-8 PubMed
Eur J Pharmacol. 1986 Oct 7;129(3):359-62 PubMed
Neuropharmacology. 1990 Jun;29(6):537-44 PubMed
Neuroscience. 1984 Jun;12(2):347-75 PubMed
