Evidence that transmitter can be released from regions of the nerve cell other than presynaptic axon terminal: Axonal release of acetylcholine without modulation

E. Vízi, K. Gyires, G. T. Somogyi, G. Ungváry

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34 Citations (Scopus)

Abstract

Release of acetylcholine from isolated preganglionic axons of sympathetic nerve trunk (cervical preganglionic sympathetic branch) of the cat was studied. In response to depolarization (KC1, 48.4 mM) acetylcholine was released into the eserinized Krebs solution. This release was shown to be dependent on extracellular Ca2+. Electrical stimulation (1 Hz) enhanced the release of acetylcholine from the isolated axonal preparation. The release by stimulation proved to be tetrodotoxin-sensitive and Ca2+-dependent. Evidence has been obtained that the acetylcholine released from sympathetic nerve trunks originates from the axon and not from Schwann cells: 5 days after section of the nerve, there was no release in response to stimulation. The release of acetylcholine from the axon is unlike that from axon terminals in that the rate of release cannot be enhanced by the inhibition of Na, K-adenosine 5′-triphosphatase (ouabain 2 × 10-5M) and cannot be modulated by noradrenaline (10-6M) or by morphine. Furthermore, although isolated nerve trunks took up [3H]choline by a hemicholinium-sensitive process, no radioactivity could be released upon electrical stimulation. It is suggested that the release of acetylcholine is not confined to axon terminals, but that it can be nonsynaptically released by depolarization from axons provided Ca2+ is present.

Original languageEnglish
Pages (from-to)967-972
Number of pages6
JournalNeuroscience
Volume10
Issue number3
DOIs
Publication statusPublished - 1983

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Presynaptic Terminals
Acetylcholine
Neurons
Axons
Electric Stimulation
Hemicholinium 3
Schwann Cells
Tetrodotoxin
Ouabain
Choline
Radioactivity
Morphine
Adenosine Triphosphatases
Norepinephrine
Cats

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

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title = "Evidence that transmitter can be released from regions of the nerve cell other than presynaptic axon terminal: Axonal release of acetylcholine without modulation",
abstract = "Release of acetylcholine from isolated preganglionic axons of sympathetic nerve trunk (cervical preganglionic sympathetic branch) of the cat was studied. In response to depolarization (KC1, 48.4 mM) acetylcholine was released into the eserinized Krebs solution. This release was shown to be dependent on extracellular Ca2+. Electrical stimulation (1 Hz) enhanced the release of acetylcholine from the isolated axonal preparation. The release by stimulation proved to be tetrodotoxin-sensitive and Ca2+-dependent. Evidence has been obtained that the acetylcholine released from sympathetic nerve trunks originates from the axon and not from Schwann cells: 5 days after section of the nerve, there was no release in response to stimulation. The release of acetylcholine from the axon is unlike that from axon terminals in that the rate of release cannot be enhanced by the inhibition of Na, K-adenosine 5′-triphosphatase (ouabain 2 × 10-5M) and cannot be modulated by noradrenaline (10-6M) or by morphine. Furthermore, although isolated nerve trunks took up [3H]choline by a hemicholinium-sensitive process, no radioactivity could be released upon electrical stimulation. It is suggested that the release of acetylcholine is not confined to axon terminals, but that it can be nonsynaptically released by depolarization from axons provided Ca2+ is present.",
author = "E. V{\'i}zi and K. Gyires and Somogyi, {G. T.} and G. Ungv{\'a}ry",
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T1 - Evidence that transmitter can be released from regions of the nerve cell other than presynaptic axon terminal

T2 - Axonal release of acetylcholine without modulation

AU - Vízi, E.

AU - Gyires, K.

AU - Somogyi, G. T.

AU - Ungváry, G.

PY - 1983

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AB - Release of acetylcholine from isolated preganglionic axons of sympathetic nerve trunk (cervical preganglionic sympathetic branch) of the cat was studied. In response to depolarization (KC1, 48.4 mM) acetylcholine was released into the eserinized Krebs solution. This release was shown to be dependent on extracellular Ca2+. Electrical stimulation (1 Hz) enhanced the release of acetylcholine from the isolated axonal preparation. The release by stimulation proved to be tetrodotoxin-sensitive and Ca2+-dependent. Evidence has been obtained that the acetylcholine released from sympathetic nerve trunks originates from the axon and not from Schwann cells: 5 days after section of the nerve, there was no release in response to stimulation. The release of acetylcholine from the axon is unlike that from axon terminals in that the rate of release cannot be enhanced by the inhibition of Na, K-adenosine 5′-triphosphatase (ouabain 2 × 10-5M) and cannot be modulated by noradrenaline (10-6M) or by morphine. Furthermore, although isolated nerve trunks took up [3H]choline by a hemicholinium-sensitive process, no radioactivity could be released upon electrical stimulation. It is suggested that the release of acetylcholine is not confined to axon terminals, but that it can be nonsynaptically released by depolarization from axons provided Ca2+ is present.

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