Glutamate stimulation of acetylcholine release from myenteric plexus is mediated by endogenous nitric oxide

Elisaveta A. Milusheva, Vjara I. Kuneva, Dimitar E. Itzev, Nadejda I. Kortezova, Beata Sperlagh, Zlatka N. Mizhorkova

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Glutamate was found to be an excitatory neurotransmitter in the enteric nervous system. Although several lines of evidence indicate a role of glutamate in the regulation of gut motility and secretion the physiological significance of glutamatergic transmission is not clear yet. We studied the effect of glutamate on [3H]acetylcholine release and nicotinamide adenine dinucleotide phosphate-diaphorase staining in longitudinal muscle strips with attached myenteric plexus of guinea pig ileum. L-Glutamate (100 μM) significantly enhanced both the evoked [3H]acetylcholine release and the optical density of nicotinamide adenine dinucleotide phosphate-diaphorase positive neurones, i.e. the intensity of staining. The non-competitive N-methyl-D-aspartate receptor antagonist MK-801 (3 μM) abolished the stimulatory effect of L-glutamate on acetylcholine efflux. Similarly, the nitric oxide synthase inhibitor Nω-nitro-L-arginine (100 μM) significantly reduced the effect of L-glutamate on [3H]acetylcholine release and nicotinamide adenine dinucleotide phosphate-diaphorase staining. Our data suggest that endogenous nitric oxide seems to mediate the stimulatory effect of glutamate on acetylcholine release from guinea pig myenteric neurons.

Original languageEnglish
Pages (from-to)229-234
Number of pages6
JournalBrain Research Bulletin
Volume66
Issue number3
DOIs
Publication statusPublished - Aug 15 2005

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Keywords

  • Acetylcholine release
  • Glutamate
  • Guinea pig ileum
  • Myenteric plexus
  • NMDA receptor
  • Nitric oxide

ASJC Scopus subject areas

  • Neuroscience(all)

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