Nitric oxide and cyclic guanosine 3',5'-monophosphate do not alter neuropeptide release from rat sensory neurons grown in culture

J. Dymshitz, Michael Vasko

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Recent studies demonstrate that nitric oxide and cyclic guanosine 3′, 5′-monophosphate may mediate hyperalgesia induced by N-methyl-d-aspartate at the level of the spinal cord. One possible mechanism for this action is that nitric oxide increases transmitter release from the primary afferent nociceptors that synapse in the dorsal horn of the spinal cord. To address this possibility, we investigated whether various nitric oxide donors and cyclic guanosine 3′, 5′-monophosphate could alter the release of substance P and calcitonin gene-related peptide from rat sensory neurons in culture. Sodium nitroprusside (100 nM to 100 μM) had little effect on basal release of either peptide, but it significantly increased the release of substance P and calcitonin gene-related peptide induced by 50 nM capsaicin. In contrast, sodium nitroprusside did not alter release evoked by 100 nM bradykinin or 30 mM KCl. Two other nitric oxide-donating compounds, S-nitroso-N-acetylpenicillamine and 3-morpholinosydnonimine did not enhance resting or capsaicin-evoked peptide release, although they induced a marked elevation in the intracellular cyclic guanosine 3′, 5′-monophosphate levels. Pretreating the cultures with 8-bromo-cyclic guanosine 3′, 5′-monophosphate, (0.5 or 0.1 mM for 30 or 60 min) did not result in the enhancement of capsaicin-induced release from sensory neurons. Moreover, pretreating the cells with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (100 μM), abolished the rise in cyclic guanosine 3′, 5′-monophosphate induced by capsaicin without altering capsaicin-stimulated release of either peptide. These data suggest that neither nitric oxide nor cyclic guanosine 3′, 5′-monophosphate are involved in enhancing peptide release from sensory neurons and that capsaicin-induced release is not mediated by cyclic guanosine 3′,5′-monophosphate.

Original languageEnglish
Pages (from-to)1279-1286
Number of pages8
JournalNeuroscience
Volume62
Issue number4
DOIs
StatePublished - 1994

Fingerprint

Guanosine Monophosphate
Cyclic GMP
Sensory Receptor Cells
Neuropeptides
Capsaicin
Nitric Oxide
Peptides
Calcitonin Gene-Related Peptide
Nitroprusside
Substance P
S-Nitroso-N-Acetylpenicillamine
Nociceptors
Nitric Oxide Donors
Nitroarginine
Hyperalgesia
Bradykinin
Aspartic Acid
Nitric Oxide Synthase
Synapses
Spinal Cord

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Nitric oxide and cyclic guanosine 3',5'-monophosphate do not alter neuropeptide release from rat sensory neurons grown in culture. / Dymshitz, J.; Vasko, Michael.

In: Neuroscience, Vol. 62, No. 4, 1994, p. 1279-1286.

Research output: Contribution to journalArticle

@article{c4541b7350a9451e80c0a899a989b7e4,
title = "Nitric oxide and cyclic guanosine 3',5'-monophosphate do not alter neuropeptide release from rat sensory neurons grown in culture",
abstract = "Recent studies demonstrate that nitric oxide and cyclic guanosine 3′, 5′-monophosphate may mediate hyperalgesia induced by N-methyl-d-aspartate at the level of the spinal cord. One possible mechanism for this action is that nitric oxide increases transmitter release from the primary afferent nociceptors that synapse in the dorsal horn of the spinal cord. To address this possibility, we investigated whether various nitric oxide donors and cyclic guanosine 3′, 5′-monophosphate could alter the release of substance P and calcitonin gene-related peptide from rat sensory neurons in culture. Sodium nitroprusside (100 nM to 100 μM) had little effect on basal release of either peptide, but it significantly increased the release of substance P and calcitonin gene-related peptide induced by 50 nM capsaicin. In contrast, sodium nitroprusside did not alter release evoked by 100 nM bradykinin or 30 mM KCl. Two other nitric oxide-donating compounds, S-nitroso-N-acetylpenicillamine and 3-morpholinosydnonimine did not enhance resting or capsaicin-evoked peptide release, although they induced a marked elevation in the intracellular cyclic guanosine 3′, 5′-monophosphate levels. Pretreating the cultures with 8-bromo-cyclic guanosine 3′, 5′-monophosphate, (0.5 or 0.1 mM for 30 or 60 min) did not result in the enhancement of capsaicin-induced release from sensory neurons. Moreover, pretreating the cells with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (100 μM), abolished the rise in cyclic guanosine 3′, 5′-monophosphate induced by capsaicin without altering capsaicin-stimulated release of either peptide. These data suggest that neither nitric oxide nor cyclic guanosine 3′, 5′-monophosphate are involved in enhancing peptide release from sensory neurons and that capsaicin-induced release is not mediated by cyclic guanosine 3′,5′-monophosphate.",
author = "J. Dymshitz and Michael Vasko",
year = "1994",
doi = "10.1016/0306-4522(94)90359-X",
language = "English",
volume = "62",
pages = "1279--1286",
journal = "Neuroscience",
issn = "0306-4522",
publisher = "Elsevier Limited",
number = "4",

}

TY - JOUR

T1 - Nitric oxide and cyclic guanosine 3',5'-monophosphate do not alter neuropeptide release from rat sensory neurons grown in culture

AU - Dymshitz, J.

AU - Vasko, Michael

PY - 1994

Y1 - 1994

N2 - Recent studies demonstrate that nitric oxide and cyclic guanosine 3′, 5′-monophosphate may mediate hyperalgesia induced by N-methyl-d-aspartate at the level of the spinal cord. One possible mechanism for this action is that nitric oxide increases transmitter release from the primary afferent nociceptors that synapse in the dorsal horn of the spinal cord. To address this possibility, we investigated whether various nitric oxide donors and cyclic guanosine 3′, 5′-monophosphate could alter the release of substance P and calcitonin gene-related peptide from rat sensory neurons in culture. Sodium nitroprusside (100 nM to 100 μM) had little effect on basal release of either peptide, but it significantly increased the release of substance P and calcitonin gene-related peptide induced by 50 nM capsaicin. In contrast, sodium nitroprusside did not alter release evoked by 100 nM bradykinin or 30 mM KCl. Two other nitric oxide-donating compounds, S-nitroso-N-acetylpenicillamine and 3-morpholinosydnonimine did not enhance resting or capsaicin-evoked peptide release, although they induced a marked elevation in the intracellular cyclic guanosine 3′, 5′-monophosphate levels. Pretreating the cultures with 8-bromo-cyclic guanosine 3′, 5′-monophosphate, (0.5 or 0.1 mM for 30 or 60 min) did not result in the enhancement of capsaicin-induced release from sensory neurons. Moreover, pretreating the cells with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (100 μM), abolished the rise in cyclic guanosine 3′, 5′-monophosphate induced by capsaicin without altering capsaicin-stimulated release of either peptide. These data suggest that neither nitric oxide nor cyclic guanosine 3′, 5′-monophosphate are involved in enhancing peptide release from sensory neurons and that capsaicin-induced release is not mediated by cyclic guanosine 3′,5′-monophosphate.

AB - Recent studies demonstrate that nitric oxide and cyclic guanosine 3′, 5′-monophosphate may mediate hyperalgesia induced by N-methyl-d-aspartate at the level of the spinal cord. One possible mechanism for this action is that nitric oxide increases transmitter release from the primary afferent nociceptors that synapse in the dorsal horn of the spinal cord. To address this possibility, we investigated whether various nitric oxide donors and cyclic guanosine 3′, 5′-monophosphate could alter the release of substance P and calcitonin gene-related peptide from rat sensory neurons in culture. Sodium nitroprusside (100 nM to 100 μM) had little effect on basal release of either peptide, but it significantly increased the release of substance P and calcitonin gene-related peptide induced by 50 nM capsaicin. In contrast, sodium nitroprusside did not alter release evoked by 100 nM bradykinin or 30 mM KCl. Two other nitric oxide-donating compounds, S-nitroso-N-acetylpenicillamine and 3-morpholinosydnonimine did not enhance resting or capsaicin-evoked peptide release, although they induced a marked elevation in the intracellular cyclic guanosine 3′, 5′-monophosphate levels. Pretreating the cultures with 8-bromo-cyclic guanosine 3′, 5′-monophosphate, (0.5 or 0.1 mM for 30 or 60 min) did not result in the enhancement of capsaicin-induced release from sensory neurons. Moreover, pretreating the cells with the nitric oxide synthase inhibitor, NG-nitro-L-arginine (100 μM), abolished the rise in cyclic guanosine 3′, 5′-monophosphate induced by capsaicin without altering capsaicin-stimulated release of either peptide. These data suggest that neither nitric oxide nor cyclic guanosine 3′, 5′-monophosphate are involved in enhancing peptide release from sensory neurons and that capsaicin-induced release is not mediated by cyclic guanosine 3′,5′-monophosphate.

UR - http://www.scopus.com/inward/record.url?scp=0028019865&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0028019865&partnerID=8YFLogxK

U2 - 10.1016/0306-4522(94)90359-X

DO - 10.1016/0306-4522(94)90359-X

M3 - Article

VL - 62

SP - 1279

EP - 1286

JO - Neuroscience

JF - Neuroscience

SN - 0306-4522

IS - 4

ER -