Neuropeptide Y inhibits adrenergic transmitter release in cultured rat superior cervical ganglion cells by restricting the availability of calcium through a pertussis toxin-sensitive mechanism

W. F. Oellerich, D. D. Schwartz, Kafait Malik

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

Neuropeptide Y has been reported to inhibit the release of the adrenergic transmitter from sympathetic nerves in many tissues. The purpose of this study was to determine the mechanism of the inhibitory effect of neuropeptide Y on the release of the adrenergic transmitter in cultured superior cervical ganglion cells prelabeled with tritiated norepinephrine. In cultured superior cervical ganglion cells superfused with a HEPES-buffered saline, electrical field stimulation (1 Hz, 30 pulses, 1 ms, 60 V) increased the fractional overflow of tritium. Neuropeptide Y (50 nM) attenuated this depolarization-induced increase in transmitter release. The nonhydrolyzable cAMP analog, 8-(4-chlorophenylthio)cyclic AMP (100 μM) and the potassium channel blockers, tetraethylammonium chloride (1 mM) and 4-aminopyridine (300 μM) potentiated the electrically stimulated increase in fractional tritium overflow but failed to alter the inhibitory effect of neuropeptide Y on fractional tritium overflow. Increasing the calcium concentration in the superfusion fluid from 1.8 to 5.4 mM potentiated the electrically stimulated increase in fractional tritium overflow and attenuated the inhibitory effect of neuropeptide Y. Reduction of superfusion fluid calcium concentration to 0.5 mM decreased electrically stimulated fractional tritium overflow and augmented the inhibitory effect of NPY on release of tritium. The fractional release of tritium in response to the calcium ionophore, ionomycin, was not significantly altered by neuropeptide Y. In Fura-2-loaded isolated sympathetic neurites obtained from superior cervical ganglia explants, the depolarization-induced (54 mM KC1) increase in cytosolic calcium was attenuated by neuropeptide Y (50 nM). Pertussis toxin (100 ng/ml for 4 h) pretreatment abolished both the neuropeptide Y-induced decrease in electrically stimulated fractional tritium overflow and the reduction in depolarization-induced increase in cytosolic calcium. These data suggest that NPY inhibits adrenergic transmitter release in cultured superior cervical ganglion cells by decreasing the availability of calcium for the release process by a pertussis toxin-sensitive mechanism.

Original languageEnglish (US)
Pages (from-to)495-502
Number of pages8
JournalNeuroscience
Volume60
Issue number2
DOIs
StatePublished - Jan 1 1994

Fingerprint

Superior Cervical Ganglion
Tritium
Neuropeptide Y
Pertussis Toxin
Adrenergic Agents
Calcium
Potassium Channel Blockers
HEPES
4-Aminopyridine
Ionomycin
Tetraethylammonium
Calcium Ionophores
Fura-2
Neurites
Cyclic AMP
Electric Stimulation
Norepinephrine

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

@article{71e20924c80b4be0a34eb5a1fe125cfc,
title = "Neuropeptide Y inhibits adrenergic transmitter release in cultured rat superior cervical ganglion cells by restricting the availability of calcium through a pertussis toxin-sensitive mechanism",
abstract = "Neuropeptide Y has been reported to inhibit the release of the adrenergic transmitter from sympathetic nerves in many tissues. The purpose of this study was to determine the mechanism of the inhibitory effect of neuropeptide Y on the release of the adrenergic transmitter in cultured superior cervical ganglion cells prelabeled with tritiated norepinephrine. In cultured superior cervical ganglion cells superfused with a HEPES-buffered saline, electrical field stimulation (1 Hz, 30 pulses, 1 ms, 60 V) increased the fractional overflow of tritium. Neuropeptide Y (50 nM) attenuated this depolarization-induced increase in transmitter release. The nonhydrolyzable cAMP analog, 8-(4-chlorophenylthio)cyclic AMP (100 μM) and the potassium channel blockers, tetraethylammonium chloride (1 mM) and 4-aminopyridine (300 μM) potentiated the electrically stimulated increase in fractional tritium overflow but failed to alter the inhibitory effect of neuropeptide Y on fractional tritium overflow. Increasing the calcium concentration in the superfusion fluid from 1.8 to 5.4 mM potentiated the electrically stimulated increase in fractional tritium overflow and attenuated the inhibitory effect of neuropeptide Y. Reduction of superfusion fluid calcium concentration to 0.5 mM decreased electrically stimulated fractional tritium overflow and augmented the inhibitory effect of NPY on release of tritium. The fractional release of tritium in response to the calcium ionophore, ionomycin, was not significantly altered by neuropeptide Y. In Fura-2-loaded isolated sympathetic neurites obtained from superior cervical ganglia explants, the depolarization-induced (54 mM KC1) increase in cytosolic calcium was attenuated by neuropeptide Y (50 nM). Pertussis toxin (100 ng/ml for 4 h) pretreatment abolished both the neuropeptide Y-induced decrease in electrically stimulated fractional tritium overflow and the reduction in depolarization-induced increase in cytosolic calcium. These data suggest that NPY inhibits adrenergic transmitter release in cultured superior cervical ganglion cells by decreasing the availability of calcium for the release process by a pertussis toxin-sensitive mechanism.",
author = "Oellerich, {W. F.} and Schwartz, {D. D.} and Kafait Malik",
year = "1994",
month = "1",
day = "1",
doi = "10.1016/0306-4522(94)90260-7",
language = "English (US)",
volume = "60",
pages = "495--502",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "2",

}

TY - JOUR

T1 - Neuropeptide Y inhibits adrenergic transmitter release in cultured rat superior cervical ganglion cells by restricting the availability of calcium through a pertussis toxin-sensitive mechanism

AU - Oellerich, W. F.

AU - Schwartz, D. D.

AU - Malik, Kafait

PY - 1994/1/1

Y1 - 1994/1/1

N2 - Neuropeptide Y has been reported to inhibit the release of the adrenergic transmitter from sympathetic nerves in many tissues. The purpose of this study was to determine the mechanism of the inhibitory effect of neuropeptide Y on the release of the adrenergic transmitter in cultured superior cervical ganglion cells prelabeled with tritiated norepinephrine. In cultured superior cervical ganglion cells superfused with a HEPES-buffered saline, electrical field stimulation (1 Hz, 30 pulses, 1 ms, 60 V) increased the fractional overflow of tritium. Neuropeptide Y (50 nM) attenuated this depolarization-induced increase in transmitter release. The nonhydrolyzable cAMP analog, 8-(4-chlorophenylthio)cyclic AMP (100 μM) and the potassium channel blockers, tetraethylammonium chloride (1 mM) and 4-aminopyridine (300 μM) potentiated the electrically stimulated increase in fractional tritium overflow but failed to alter the inhibitory effect of neuropeptide Y on fractional tritium overflow. Increasing the calcium concentration in the superfusion fluid from 1.8 to 5.4 mM potentiated the electrically stimulated increase in fractional tritium overflow and attenuated the inhibitory effect of neuropeptide Y. Reduction of superfusion fluid calcium concentration to 0.5 mM decreased electrically stimulated fractional tritium overflow and augmented the inhibitory effect of NPY on release of tritium. The fractional release of tritium in response to the calcium ionophore, ionomycin, was not significantly altered by neuropeptide Y. In Fura-2-loaded isolated sympathetic neurites obtained from superior cervical ganglia explants, the depolarization-induced (54 mM KC1) increase in cytosolic calcium was attenuated by neuropeptide Y (50 nM). Pertussis toxin (100 ng/ml for 4 h) pretreatment abolished both the neuropeptide Y-induced decrease in electrically stimulated fractional tritium overflow and the reduction in depolarization-induced increase in cytosolic calcium. These data suggest that NPY inhibits adrenergic transmitter release in cultured superior cervical ganglion cells by decreasing the availability of calcium for the release process by a pertussis toxin-sensitive mechanism.

AB - Neuropeptide Y has been reported to inhibit the release of the adrenergic transmitter from sympathetic nerves in many tissues. The purpose of this study was to determine the mechanism of the inhibitory effect of neuropeptide Y on the release of the adrenergic transmitter in cultured superior cervical ganglion cells prelabeled with tritiated norepinephrine. In cultured superior cervical ganglion cells superfused with a HEPES-buffered saline, electrical field stimulation (1 Hz, 30 pulses, 1 ms, 60 V) increased the fractional overflow of tritium. Neuropeptide Y (50 nM) attenuated this depolarization-induced increase in transmitter release. The nonhydrolyzable cAMP analog, 8-(4-chlorophenylthio)cyclic AMP (100 μM) and the potassium channel blockers, tetraethylammonium chloride (1 mM) and 4-aminopyridine (300 μM) potentiated the electrically stimulated increase in fractional tritium overflow but failed to alter the inhibitory effect of neuropeptide Y on fractional tritium overflow. Increasing the calcium concentration in the superfusion fluid from 1.8 to 5.4 mM potentiated the electrically stimulated increase in fractional tritium overflow and attenuated the inhibitory effect of neuropeptide Y. Reduction of superfusion fluid calcium concentration to 0.5 mM decreased electrically stimulated fractional tritium overflow and augmented the inhibitory effect of NPY on release of tritium. The fractional release of tritium in response to the calcium ionophore, ionomycin, was not significantly altered by neuropeptide Y. In Fura-2-loaded isolated sympathetic neurites obtained from superior cervical ganglia explants, the depolarization-induced (54 mM KC1) increase in cytosolic calcium was attenuated by neuropeptide Y (50 nM). Pertussis toxin (100 ng/ml for 4 h) pretreatment abolished both the neuropeptide Y-induced decrease in electrically stimulated fractional tritium overflow and the reduction in depolarization-induced increase in cytosolic calcium. These data suggest that NPY inhibits adrenergic transmitter release in cultured superior cervical ganglion cells by decreasing the availability of calcium for the release process by a pertussis toxin-sensitive mechanism.

UR - http://www.scopus.com/inward/record.url?scp=0028357945&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028357945&partnerID=8YFLogxK

U2 - 10.1016/0306-4522(94)90260-7

DO - 10.1016/0306-4522(94)90260-7

M3 - Article

VL - 60

SP - 495

EP - 502

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 2

ER -