Release of acetylcholine from rat brain synaptosomes by various agents in the absence of external calcium ions.

Research output: Contribution to journalArticle

76 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)505-521
Number of pages17
JournalJournal of Physiology
Volume353
Issue number1
DOIs
Publication statusPublished - Aug 1 1984

Fingerprint

Synaptosomes
Veratridine
Acetylcholine
Ouabain
Ions
Calcium
Brain
Membrane Potentials
Ionophores
Calcimycin
Membranes

ASJC Scopus subject areas

  • Physiology

Cite this

@article{a7becdd94c9949bc95f5b50032d0a43c,
title = "Release of acetylcholine from rat brain synaptosomes by various agents in the absence of external calcium ions.",
abstract = "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.",
author = "V. {\'A}d{\'a}m-Vizi and E. Ligeti",
year = "1984",
month = "8",
day = "1",
doi = "10.1113/jphysiol.1984.sp015348",
language = "English",
volume = "353",
pages = "505--521",
journal = "Journal of Physiology",
issn = "0022-3751",
publisher = "Wiley-Blackwell",
number = "1",

}

TY - JOUR

T1 - Release of acetylcholine from rat brain synaptosomes by various agents in the absence of external calcium ions.

AU - Ádám-Vizi, V.

AU - Ligeti, E.

PY - 1984/8/1

Y1 - 1984/8/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0021284541&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0021284541&partnerID=8YFLogxK

U2 - 10.1113/jphysiol.1984.sp015348

DO - 10.1113/jphysiol.1984.sp015348

M3 - Article

C2 - 6090643

AN - SCOPUS:0021284541

VL - 353

SP - 505

EP - 521

JO - Journal of Physiology

JF - Journal of Physiology

SN - 0022-3751

IS - 1

ER -