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 N ω-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.
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