Release of acetylcholine from rat brain synaptosomes by various agents in the absence of external calcium ions
The relationship between 86Rb+ distribution across synaptosomal membrane and [14C]acetylcholine (ACh) release have been studied in a rat brain cortex synaptosomal preparation using K+, ouabain and veratridine depolarization. Decrease in membrane potential, approximated from the 86Rb+ distribution, i...
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Published in | The Journal of physiology Vol. 353; no. 1; pp. 505 - 521 |
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Main Authors | , |
Format | Journal Article |
Language | English |
Published |
Oxford
The Physiological Society
01.08.1984
Blackwell |
Subjects | |
Online Access | Get full text |
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Summary: | The relationship between 86Rb+ distribution across synaptosomal membrane and [14C]acetylcholine (ACh) release have been studied
in a rat brain cortex synaptosomal preparation using K+, ouabain and veratridine depolarization. Decrease in membrane potential,
approximated from the 86Rb+ distribution, is accompanied by an increase in [14C]ACh release, but the extent of the increase
at a certain depolarization is dependent on how the depolarization is induced. A substantial depolarization by K+ is necessary
to enhance ACh release, as compared to ouabain and veratridine where only a slight depolarization is accompanied by an increase
in ACh release. In Ca2+-free, EGTA-containing medium ouabain and veratridine can also increase [14C]ACh release. The relationship
between membrane potential and ACh release is very similar in the presence of ouabain and veratridine both in Ca2+-containing
and Ca2+-free medium. The effect of ouabain and veratridine on the Na-K exchange pump is different; ouabain can completely
abolish Na-K-ATPase activity and 86Rb+ uptake of synaptosomes, whereas veratridine does not seem to influence the activity
of the pump. m-Chloro-carbonylcianid phenyl hydrazon (50-500 nM) increases [14C]ACh release in a concentration-dependent manner
without a considerable change of membrane potential or Na-K pump activity. The Ca2+ ionophore A 23187 induces a substantial
increase in [14C]ACh release in the absence of external Ca2+. In this case neither Na-K pump activity nor membrane potential
of synaptosomes is changed. A possible role of intracellular Ca2+ mobilization as a consequence of increased intracellular
Na+ concentration in some depolarization-induced transmitter release is discussed. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.1984.sp015348 |