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

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 microM) 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 microM) abolished the stimulatory effect of L-glutamate on acetylcholine efflux. Similarly, the nitric oxide synthase inhibitor N(omega)-nitro-L-arginine (100 microM) 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.

journal_name

Brain Res Bull

journal_title

Brain research bulletin

authors

Milusheva EA,Kuneva VI,Itzev DE,Kortezova NI,Sperlagh B,Mizhorkova ZN

doi

10.1016/j.brainresbull.2005.05.011

keywords:

subject

Has Abstract

pub_date

2005-08-15 00:00:00

pages

229-34

issue

3

eissn

0361-9230

issn

1873-2747

pii

S0361-9230(05)00194-2

journal_volume

66

pub_type

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