Nitric oxide increases stimulation-evoked acetylcholine release from rat hippocampal slices by a cyclic GMP-independent mechanism

Takeshi Suzuki, Kaori Nakajima, Kazuko Fujimoto, Takeshi Fujii, Koichiro Kawashima

Research output: Contribution to journalArticle

18 Citations (Scopus)

Abstract

Nitric oxide (NO) is an endothelium-derived relaxing factor and its main mechanism of action is activation of soluble guanylyl cyclase. NO and NO- related compounds have been reported to affect several neuronal functions in the central nervous system. In this study, we investigated the effects of NO donors (sodium nitroprusside (SNP) and (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]- 5-nitro-3-hexenamide (FK409)) on acetylcholine (ACh) release from rat hippocampal slices. SNP (10-5 M) and FK409 (10-4 M) increased electrical stimulation-evoked ACh release without affecting basal release. As dibutyryl cyclic GMP inhibited stimulation-evoked ACh release, the effects of these NO donors were not due to soluble guanylyl cyclase activation. Atropine increased stimulation-evoked ACh release by blocking presynaptic muscarinic autoreceptors, and SNP increased stimulation-evoked ACh release in the presence of atropine, suggesting that SNP and atropine increase stimulation- evoked ACh release by different mechanisms. The present results indicate that NO enhances some part of the excitation-secretion coupling pathway without inducing ACh release directly and these effects are mediated by cyclic GMP- independent mechanism.

Original languageEnglish
Pages (from-to)158-162
Number of pages5
JournalBrain Research
Volume760
Issue number1-2
DOIs
Publication statusPublished - 1997 Jun 20

Fingerprint

Cyclic GMP
Acetylcholine
Nitric Oxide
Nitroprusside
Atropine
Nitric Oxide Donors
Dibutyryl Cyclic GMP
Endothelium-Dependent Relaxing Factors
Autoreceptors
Secretory Pathway
Cholinergic Agents
Electric Stimulation
Central Nervous System

Keywords

  • Acetylcholine release
  • Autoinhibition
  • Choline
  • Cyclic GMP
  • Hippocampus
  • Nitric oxide (NO)

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

Nitric oxide increases stimulation-evoked acetylcholine release from rat hippocampal slices by a cyclic GMP-independent mechanism. / Suzuki, Takeshi; Nakajima, Kaori; Fujimoto, Kazuko; Fujii, Takeshi; Kawashima, Koichiro.

In: Brain Research, Vol. 760, No. 1-2, 20.06.1997, p. 158-162.

Research output: Contribution to journalArticle

@article{2b54db302efb4c3fb0c792ed8ce52140,
title = "Nitric oxide increases stimulation-evoked acetylcholine release from rat hippocampal slices by a cyclic GMP-independent mechanism",
abstract = "Nitric oxide (NO) is an endothelium-derived relaxing factor and its main mechanism of action is activation of soluble guanylyl cyclase. NO and NO- related compounds have been reported to affect several neuronal functions in the central nervous system. In this study, we investigated the effects of NO donors (sodium nitroprusside (SNP) and (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]- 5-nitro-3-hexenamide (FK409)) on acetylcholine (ACh) release from rat hippocampal slices. SNP (10-5 M) and FK409 (10-4 M) increased electrical stimulation-evoked ACh release without affecting basal release. As dibutyryl cyclic GMP inhibited stimulation-evoked ACh release, the effects of these NO donors were not due to soluble guanylyl cyclase activation. Atropine increased stimulation-evoked ACh release by blocking presynaptic muscarinic autoreceptors, and SNP increased stimulation-evoked ACh release in the presence of atropine, suggesting that SNP and atropine increase stimulation- evoked ACh release by different mechanisms. The present results indicate that NO enhances some part of the excitation-secretion coupling pathway without inducing ACh release directly and these effects are mediated by cyclic GMP- independent mechanism.",
keywords = "Acetylcholine release, Autoinhibition, Choline, Cyclic GMP, Hippocampus, Nitric oxide (NO)",
author = "Takeshi Suzuki and Kaori Nakajima and Kazuko Fujimoto and Takeshi Fujii and Koichiro Kawashima",
year = "1997",
month = "6",
day = "20",
doi = "10.1016/S0006-8993(97)00291-6",
language = "English",
volume = "760",
pages = "158--162",
journal = "Brain Research",
issn = "0006-8993",
publisher = "Elsevier",
number = "1-2",

}

TY - JOUR

T1 - Nitric oxide increases stimulation-evoked acetylcholine release from rat hippocampal slices by a cyclic GMP-independent mechanism

AU - Suzuki, Takeshi

AU - Nakajima, Kaori

AU - Fujimoto, Kazuko

AU - Fujii, Takeshi

AU - Kawashima, Koichiro

PY - 1997/6/20

Y1 - 1997/6/20

N2 - Nitric oxide (NO) is an endothelium-derived relaxing factor and its main mechanism of action is activation of soluble guanylyl cyclase. NO and NO- related compounds have been reported to affect several neuronal functions in the central nervous system. In this study, we investigated the effects of NO donors (sodium nitroprusside (SNP) and (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]- 5-nitro-3-hexenamide (FK409)) on acetylcholine (ACh) release from rat hippocampal slices. SNP (10-5 M) and FK409 (10-4 M) increased electrical stimulation-evoked ACh release without affecting basal release. As dibutyryl cyclic GMP inhibited stimulation-evoked ACh release, the effects of these NO donors were not due to soluble guanylyl cyclase activation. Atropine increased stimulation-evoked ACh release by blocking presynaptic muscarinic autoreceptors, and SNP increased stimulation-evoked ACh release in the presence of atropine, suggesting that SNP and atropine increase stimulation- evoked ACh release by different mechanisms. The present results indicate that NO enhances some part of the excitation-secretion coupling pathway without inducing ACh release directly and these effects are mediated by cyclic GMP- independent mechanism.

AB - Nitric oxide (NO) is an endothelium-derived relaxing factor and its main mechanism of action is activation of soluble guanylyl cyclase. NO and NO- related compounds have been reported to affect several neuronal functions in the central nervous system. In this study, we investigated the effects of NO donors (sodium nitroprusside (SNP) and (±)-(E)-4-ethyl-2-[(E)-hydroxyimino]- 5-nitro-3-hexenamide (FK409)) on acetylcholine (ACh) release from rat hippocampal slices. SNP (10-5 M) and FK409 (10-4 M) increased electrical stimulation-evoked ACh release without affecting basal release. As dibutyryl cyclic GMP inhibited stimulation-evoked ACh release, the effects of these NO donors were not due to soluble guanylyl cyclase activation. Atropine increased stimulation-evoked ACh release by blocking presynaptic muscarinic autoreceptors, and SNP increased stimulation-evoked ACh release in the presence of atropine, suggesting that SNP and atropine increase stimulation- evoked ACh release by different mechanisms. The present results indicate that NO enhances some part of the excitation-secretion coupling pathway without inducing ACh release directly and these effects are mediated by cyclic GMP- independent mechanism.

KW - Acetylcholine release

KW - Autoinhibition

KW - Choline

KW - Cyclic GMP

KW - Hippocampus

KW - Nitric oxide (NO)

UR - http://www.scopus.com/inward/record.url?scp=0030737978&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0030737978&partnerID=8YFLogxK

U2 - 10.1016/S0006-8993(97)00291-6

DO - 10.1016/S0006-8993(97)00291-6

M3 - Article

C2 - 9237530

AN - SCOPUS:0030737978

VL - 760

SP - 158

EP - 162

JO - Brain Research

JF - Brain Research

SN - 0006-8993

IS - 1-2

ER -