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

Keywords

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

ASJC Scopus subject areas

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

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