Inhibitory effect of dopamine on acetylcholine release from caudate nucleus

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Abstract

It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6 hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.

Original languageEnglish
Pages (from-to)201-211
Number of pages11
JournalPolish Journal of Pharmacology and Pharmacy
Volume29
Issue number3
Publication statusPublished - 1977

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Caudate Nucleus
Cholinergic Agents
Acetylcholine
Dopamine
Neurosecretion
Hyperkinesis
Corpus Striatum
Oxidopamine
Reserpine
Chlorpromazine
Interneurons
Haloperidol
Pharmaceutical Preparations

ASJC Scopus subject areas

  • Pharmaceutical Science
  • Pharmacology

Cite this

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title = "Inhibitory effect of dopamine on acetylcholine release from caudate nucleus",
abstract = "It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6 hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.",
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AU - Vízi, E.

AU - Rónai, A.

AU - Hársing, L.

AU - Knoll, J.

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N2 - It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6 hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.

AB - It has been shown that dopamine inhibits the release of acetylcholine (ACh) from nerve terminals of caudate cholinergic interneurons, and the imbalance between dopaminergic and cholinergic system by 6 hydroxydopamine pretreatment leads to an increased ACh release. The Parkinson syndrome induced by drugs which depress dopaminergic function either by reducing the output of dopamine, such as reserpine, or by antagonizing its action on DA receptors, as for instance haloperidol or chlorpromazine, can be attributed to the augmented release of ACh from caudate cholinergic nerve terminals and a consequent increase of cholinergic outflow from caudate nucleus. However, athetoid and choreiform hyperkinesis in patients and hypermotility in animals might result from increased dopaminergic outflow of nigro striatal pathway and a consequent reduction in cholinergic neurosecretion of caudate nucleus.

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