In vitro and in vivo evidence of neurotensin release from preganglionic axon terminals in the stellate ganglion of the cat

E. Maher, B. Bachoo, C. Polosa

Research output: Contribution to journalArticle

8 Citations (Scopus)

Abstract

We have previously shown that the neurotensin (NT) store in preganglionic axon terminals of the cat stellate ganglion (SG) is reversibly depleted by prolonged preganglionic stimulation. The present study addresses the questions of whether the preganglionic axon terminals release NT in response to depolarizing stimuli in vitro and whether in vivo NT is released by the tonic firing of the sympathetic preganglionic neurons. Slices of the SG of the anaesthetized cat, maintained in oxygenated Ringer solution, released NT. The efflux increased when the K concentration was increased from 5 to 25 or 45 mM or when veratridine was added to the medium. In Ca-free medium, efflux was suppressed. The effect of veratridine was blocked by tetrodotoxin (TTX). In awake, freely moving cats, in which TTX was applied for 4 days to the preganglionic input of the right SG, the NT content of this ganglion doubled by comparison with the left SG. Since NT accumulates proximal to a ligature on the preganglionic input of the SG, the increased NT content is likely to result from suppression of action potential-dependent release while influx into the terminals persists. This result suggests that the steady state of the NT store in sympathetic preganglionic terminals is the result of a steady influx from the soma balanced by action potential-dependent loss, presumably release.

Original languageEnglish (US)
Pages (from-to)131-135
Number of pages5
JournalBrain Research
Volume640
Issue number1-2
DOIs
StatePublished - Mar 21 1994

Fingerprint

Stellate Ganglion
Neurotensin
Presynaptic Terminals
Cats
Veratridine
Tetrodotoxin
Action Potentials
In Vitro Techniques
Carisoprodol
Ganglia
Ligation
Neurons

Keywords

  • Neuropeptide release
  • Neuropeptide turnover
  • Preganglionic neuron
  • Sympathetic ganglion
  • Tonic activity

ASJC Scopus subject areas

  • Developmental Biology
  • Molecular Biology
  • Clinical Neurology
  • Neuroscience(all)

Cite this

In vitro and in vivo evidence of neurotensin release from preganglionic axon terminals in the stellate ganglion of the cat. / Maher, E.; Bachoo, B.; Polosa, C.

In: Brain Research, Vol. 640, No. 1-2, 21.03.1994, p. 131-135.

Research output: Contribution to journalArticle

@article{f493f1dc422a4c13a55434fb82dd8030,
title = "In vitro and in vivo evidence of neurotensin release from preganglionic axon terminals in the stellate ganglion of the cat",
abstract = "We have previously shown that the neurotensin (NT) store in preganglionic axon terminals of the cat stellate ganglion (SG) is reversibly depleted by prolonged preganglionic stimulation. The present study addresses the questions of whether the preganglionic axon terminals release NT in response to depolarizing stimuli in vitro and whether in vivo NT is released by the tonic firing of the sympathetic preganglionic neurons. Slices of the SG of the anaesthetized cat, maintained in oxygenated Ringer solution, released NT. The efflux increased when the K concentration was increased from 5 to 25 or 45 mM or when veratridine was added to the medium. In Ca-free medium, efflux was suppressed. The effect of veratridine was blocked by tetrodotoxin (TTX). In awake, freely moving cats, in which TTX was applied for 4 days to the preganglionic input of the right SG, the NT content of this ganglion doubled by comparison with the left SG. Since NT accumulates proximal to a ligature on the preganglionic input of the SG, the increased NT content is likely to result from suppression of action potential-dependent release while influx into the terminals persists. This result suggests that the steady state of the NT store in sympathetic preganglionic terminals is the result of a steady influx from the soma balanced by action potential-dependent loss, presumably release.",
keywords = "Neuropeptide release, Neuropeptide turnover, Preganglionic neuron, Sympathetic ganglion, Tonic activity",
author = "E. Maher and B. Bachoo and C. Polosa",
year = "1994",
month = "3",
day = "21",
doi = "10.1016/0006-8993(94)91866-X",
language = "English (US)",
volume = "640",
pages = "131--135",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - In vitro and in vivo evidence of neurotensin release from preganglionic axon terminals in the stellate ganglion of the cat

AU - Maher, E.

AU - Bachoo, B.

AU - Polosa, C.

PY - 1994/3/21

Y1 - 1994/3/21

N2 - We have previously shown that the neurotensin (NT) store in preganglionic axon terminals of the cat stellate ganglion (SG) is reversibly depleted by prolonged preganglionic stimulation. The present study addresses the questions of whether the preganglionic axon terminals release NT in response to depolarizing stimuli in vitro and whether in vivo NT is released by the tonic firing of the sympathetic preganglionic neurons. Slices of the SG of the anaesthetized cat, maintained in oxygenated Ringer solution, released NT. The efflux increased when the K concentration was increased from 5 to 25 or 45 mM or when veratridine was added to the medium. In Ca-free medium, efflux was suppressed. The effect of veratridine was blocked by tetrodotoxin (TTX). In awake, freely moving cats, in which TTX was applied for 4 days to the preganglionic input of the right SG, the NT content of this ganglion doubled by comparison with the left SG. Since NT accumulates proximal to a ligature on the preganglionic input of the SG, the increased NT content is likely to result from suppression of action potential-dependent release while influx into the terminals persists. This result suggests that the steady state of the NT store in sympathetic preganglionic terminals is the result of a steady influx from the soma balanced by action potential-dependent loss, presumably release.

AB - We have previously shown that the neurotensin (NT) store in preganglionic axon terminals of the cat stellate ganglion (SG) is reversibly depleted by prolonged preganglionic stimulation. The present study addresses the questions of whether the preganglionic axon terminals release NT in response to depolarizing stimuli in vitro and whether in vivo NT is released by the tonic firing of the sympathetic preganglionic neurons. Slices of the SG of the anaesthetized cat, maintained in oxygenated Ringer solution, released NT. The efflux increased when the K concentration was increased from 5 to 25 or 45 mM or when veratridine was added to the medium. In Ca-free medium, efflux was suppressed. The effect of veratridine was blocked by tetrodotoxin (TTX). In awake, freely moving cats, in which TTX was applied for 4 days to the preganglionic input of the right SG, the NT content of this ganglion doubled by comparison with the left SG. Since NT accumulates proximal to a ligature on the preganglionic input of the SG, the increased NT content is likely to result from suppression of action potential-dependent release while influx into the terminals persists. This result suggests that the steady state of the NT store in sympathetic preganglionic terminals is the result of a steady influx from the soma balanced by action potential-dependent loss, presumably release.

KW - Neuropeptide release

KW - Neuropeptide turnover

KW - Preganglionic neuron

KW - Sympathetic ganglion

KW - Tonic activity

UR - http://www.scopus.com/inward/record.url?scp=0028351225&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028351225&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(94)91866-X

DO - 10.1016/0006-8993(94)91866-X

M3 - Article

C2 - 8004441

AN - SCOPUS:0028351225

VL - 640

SP - 131

EP - 135

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -