Prostacyclin enhances the evoked-release of substance P and calcitonin gene-related peptide from rat sensory neurons

Cynthia M. Hingtgen, Michael Vasko

Research output: Contribution to journalArticle

91 Citations (Scopus)

Abstract

Prostacyclin (PGI2) is a potent prostanoid producing various symptoms of inflammation, including an increased sensitivity to noxious stimulation. One component of these PGI2-mediated actions may involve activation or sensitization of sensory neurons to enhance release of neuroactive peptides. We, therefore, examined whether PGI2 and carra prostacyclin (CPGI2), a stable analog of PGI2, could alter the resting and evoked release of the neuropeptides, substance P (SP) and calcitonin gene-related peptide (CGRP) from embryonic rat sensory neurons grown in culture. Treating isolated sensory neurons with CPGI2 (10-1000 nM) for 30 min caused a 3-fold increase in the resting release of both peptides. One nM CPGI2, a concentration that did not alter the resting release, significantly enhanced neuropeptide release evoked by capsaicin, 100 nM bradykinin, or 40 mM KCl. Similarly, 10 nM PGI2 did not alter resting release, but augmented capsaicin-stimulated release of SP and CGRP 2-3 fold. In contrast, prostaglandin F was ineffective in altering either resting or capsaicin-evoked peptide release. Our results demonstrate that low concentrations of PGI2 sensitize sensory neurons to other stimuli, whereas higher concentrations evoke release directly. This PGI2-induced augmentation of neuropeptide release may be one mechanism contributing to neurogenic inflammation.

Original languageEnglish
Pages (from-to)51-60
Number of pages10
JournalBrain Research
Volume655
Issue number1-2
DOIs
StatePublished - Aug 29 1994

Fingerprint

Calcitonin Gene-Related Peptide
Sensory Receptor Cells
Epoprostenol
Substance P
Capsaicin
Neuropeptides
Peptides
Neurogenic Inflammation
Dinoprost
Bradykinin
Prostaglandins
Inflammation

Keywords

  • Bradykinin
  • Capsaicin
  • Dorsal root ganglia
  • Prostaglandin
  • Sensory neuron

ASJC Scopus subject areas

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

Cite this

Prostacyclin enhances the evoked-release of substance P and calcitonin gene-related peptide from rat sensory neurons. / Hingtgen, Cynthia M.; Vasko, Michael.

In: Brain Research, Vol. 655, No. 1-2, 29.08.1994, p. 51-60.

Research output: Contribution to journalArticle

@article{47d8e701d452423dabb0ea3817c6bb42,
title = "Prostacyclin enhances the evoked-release of substance P and calcitonin gene-related peptide from rat sensory neurons",
abstract = "Prostacyclin (PGI2) is a potent prostanoid producing various symptoms of inflammation, including an increased sensitivity to noxious stimulation. One component of these PGI2-mediated actions may involve activation or sensitization of sensory neurons to enhance release of neuroactive peptides. We, therefore, examined whether PGI2 and carra prostacyclin (CPGI2), a stable analog of PGI2, could alter the resting and evoked release of the neuropeptides, substance P (SP) and calcitonin gene-related peptide (CGRP) from embryonic rat sensory neurons grown in culture. Treating isolated sensory neurons with CPGI2 (10-1000 nM) for 30 min caused a 3-fold increase in the resting release of both peptides. One nM CPGI2, a concentration that did not alter the resting release, significantly enhanced neuropeptide release evoked by capsaicin, 100 nM bradykinin, or 40 mM KCl. Similarly, 10 nM PGI2 did not alter resting release, but augmented capsaicin-stimulated release of SP and CGRP 2-3 fold. In contrast, prostaglandin F2α was ineffective in altering either resting or capsaicin-evoked peptide release. Our results demonstrate that low concentrations of PGI2 sensitize sensory neurons to other stimuli, whereas higher concentrations evoke release directly. This PGI2-induced augmentation of neuropeptide release may be one mechanism contributing to neurogenic inflammation.",
keywords = "Bradykinin, Capsaicin, Dorsal root ganglia, Prostaglandin, Sensory neuron",
author = "Hingtgen, {Cynthia M.} and Michael Vasko",
year = "1994",
month = "8",
day = "29",
doi = "10.1016/0006-8993(94)91596-2",
language = "English",
volume = "655",
pages = "51--60",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Prostacyclin enhances the evoked-release of substance P and calcitonin gene-related peptide from rat sensory neurons

AU - Hingtgen, Cynthia M.

AU - Vasko, Michael

PY - 1994/8/29

Y1 - 1994/8/29

N2 - Prostacyclin (PGI2) is a potent prostanoid producing various symptoms of inflammation, including an increased sensitivity to noxious stimulation. One component of these PGI2-mediated actions may involve activation or sensitization of sensory neurons to enhance release of neuroactive peptides. We, therefore, examined whether PGI2 and carra prostacyclin (CPGI2), a stable analog of PGI2, could alter the resting and evoked release of the neuropeptides, substance P (SP) and calcitonin gene-related peptide (CGRP) from embryonic rat sensory neurons grown in culture. Treating isolated sensory neurons with CPGI2 (10-1000 nM) for 30 min caused a 3-fold increase in the resting release of both peptides. One nM CPGI2, a concentration that did not alter the resting release, significantly enhanced neuropeptide release evoked by capsaicin, 100 nM bradykinin, or 40 mM KCl. Similarly, 10 nM PGI2 did not alter resting release, but augmented capsaicin-stimulated release of SP and CGRP 2-3 fold. In contrast, prostaglandin F2α was ineffective in altering either resting or capsaicin-evoked peptide release. Our results demonstrate that low concentrations of PGI2 sensitize sensory neurons to other stimuli, whereas higher concentrations evoke release directly. This PGI2-induced augmentation of neuropeptide release may be one mechanism contributing to neurogenic inflammation.

AB - Prostacyclin (PGI2) is a potent prostanoid producing various symptoms of inflammation, including an increased sensitivity to noxious stimulation. One component of these PGI2-mediated actions may involve activation or sensitization of sensory neurons to enhance release of neuroactive peptides. We, therefore, examined whether PGI2 and carra prostacyclin (CPGI2), a stable analog of PGI2, could alter the resting and evoked release of the neuropeptides, substance P (SP) and calcitonin gene-related peptide (CGRP) from embryonic rat sensory neurons grown in culture. Treating isolated sensory neurons with CPGI2 (10-1000 nM) for 30 min caused a 3-fold increase in the resting release of both peptides. One nM CPGI2, a concentration that did not alter the resting release, significantly enhanced neuropeptide release evoked by capsaicin, 100 nM bradykinin, or 40 mM KCl. Similarly, 10 nM PGI2 did not alter resting release, but augmented capsaicin-stimulated release of SP and CGRP 2-3 fold. In contrast, prostaglandin F2α was ineffective in altering either resting or capsaicin-evoked peptide release. Our results demonstrate that low concentrations of PGI2 sensitize sensory neurons to other stimuli, whereas higher concentrations evoke release directly. This PGI2-induced augmentation of neuropeptide release may be one mechanism contributing to neurogenic inflammation.

KW - Bradykinin

KW - Capsaicin

KW - Dorsal root ganglia

KW - Prostaglandin

KW - Sensory neuron

UR - http://www.scopus.com/inward/record.url?scp=0028021668&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028021668&partnerID=8YFLogxK

U2 - 10.1016/0006-8993(94)91596-2

DO - 10.1016/0006-8993(94)91596-2

M3 - Article

C2 - 7529126

AN - SCOPUS:0028021668

VL - 655

SP - 51

EP - 60

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -