Colocalization of nitric oxide synthase and NADPH-diaphorase in the myenteric plexus of the rat gut

Belai, Abebech; Schmidt, Harald; Hoyle, Charles H.V.; Hassall, C. J. S.; Saffrey, M. Jill; Moss, Jonathan; Förstermann, Ulrich; Murad, Ferid; Burnstock, Geoffrey

doi:10.1016/0304-3940(92)90233-w

Cited by 197 publications

(70 citation statements)

References 16 publications

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“…Thus, functions of the ganglia were analyzed by examining the production of NADPH diaphorase and substance P in the neuronal cells. NADPH diaphorase is identical to nitric oxide synthase (26)(27)(28)(29) and nitric oxide functions as an inhibitory neurotransmitter to relax smooth muscle (30), while substance P is an excitatory neurotransmitter to contract circular smooth muscles (31,32). NADPH diaphorase positive neuronal cells were dense in the proximal colon of Ncx Ϫ / Ϫ mice with (data not shown) or without megacolon (Fig.…”

Section: Resultsmentioning

confidence: 83%

A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice.

Hatano¹,

Aoki²,

Dezawa³

et al. 1997

J. Clin. Invest.

110

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The Ncx/Hox11L.1 gene, a member of the Hox11 homeobox gene family, is mainly expressed in neural crest-derived tissues. To elucidate the role of Ncx/Hox11L.1, the gene has been inactivated in embryonic stem cells by homologous recombination. The homozygous mutant mice were viable. These mice developed megacolon with enteric ganglia by age 3-5 wk. Histochemical analysis of the ganglia revealed that the enteric neurons hyperinnervated in the narrow segment of megacolon. Some of these neuronal cells degenerated and neuronal cell death occurred in later stages. We propose that Ncx/Hox11L.1 is required for maintenance of proper functions of the enteric nervous system. These mutant mice can be used to elucidate a novel pathogenesis for human neuronal intestinal dysplasia. ( J. Clin. Invest. 1997. 100:795-801.)

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Section: Resultsmentioning

confidence: 83%

A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice.

Hatano¹,

Aoki²,

Dezawa³

et al. 1997

J. Clin. Invest.

110

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“…Thus, NOS immunoreactivity and NADPH diaphorase enzyme activity correspond 100% in the myenteric neurons of the trout as they do in mammals, amphibians and birds (BELAI et al, 1992;LI et al, 1992LI et al, , 1993WARD et al, 1992;YOUNG et al, 1992). There are several possible explanations for the lack of NOS immunoreactivity in some nerve cell bodies of the vagus.…”

Section: Discussionmentioning

confidence: 91%

“…In the central and enteric nervous system of mammals, NOS immunoreactivity is co-localized with NADPH diaphorase staining, and it has been suggested that NADPH diaphorase reactivity reveals the NADPH binding site of NOS (DAWSON et al, 1991;HOPE et al, 1991;BELAI et al, 1992;WARD et al, 1992;YOUNG et al, 1992). A similar one-to-one correlation between the NOS immunoreactivity and NADPH diaphorase staining has been noted to occur in neurons of the myenteric and submucous plexuses of the gastrointestinal tract of both an amphibian and a bird (LI et al, , 1993.…”

mentioning

confidence: 91%

Nitric oxide synthase in the enteric nervous system of the rainbow trout, Salmo gairdneri .

Furness

1993

Archives of Histology and Cytology

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Summary. The distribution of nitric oxide synthase (NOS) was determined in the gastrointestinal tract of the rainbow trout, Salmo gairdneri. NOS immunoreactivity and the NADPH diaphorase histochemical reaction were co-localized in nerve cells in the myenteric ganglia. However, only about 60% of NADPH diaphorase-stained nerve cells in the vagus nerve trunks were immunoreactive for NOS. Reactive myenteric nerve cells were found throughout the gastrointestinal tract, comprising about 10-15% of all nerve cells. Reactive nerve cells and fibres appeared in the myenteric ganglia and nerve trunks. The circular muscle was innervated by reactive nerve fibres throughout the gastrointestinal tract. Some NOS-containing cell bodies were also in this layer. The submucous plexus contained reactive nerve fibres in each region of the gut; in the large intestine a few reactive nerve cell bodies were also seen in this plexus. The muscle in the mucosal folds of the large intestine was densely innervated. The observations suggest that nitric oxide is an enteric transmitter in teleost fish, as it is in mammals.

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“…NO released from neurones has been suggested as a non-adrenergic non-cholinergic (NANC) mediator of relaxation in intestinal smooth muscle (Bult et al, 1990;Desai et al, 1991). In support, NO synthase is present within enteric neurones (Bredt et al, 1991;Belai et al, 1992;Ward et al, 1992) and nerve-stimulation elicits the release of a factor with similar biological activity to NO (Bult et al, 1990;Wiklund et al, 1993). Furthermore, nerve-stimulation induces a frequency-dependent release of the NO-metabolites, nitrite and nitrate in guinea-pig intestine (Wiklund et al, 1993).…”

Section: Introductionmentioning

confidence: 98%

Smooth muscle relaxing effects of NO, nitrosothiols and a nerve‐induced relaxing factor released in guinea‐pig colon

Iversen

Gustafsson

Leone

et al. 1994

British J Pharmacology

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Institute, S-171 77 Stockholm, Sweden and **Wellcome Research Laboratories, Langley Court, Beckenham, Kent BR3 3BS 1 The aim of the present study was to compare the biological activity of S-nitroso-L-cysteine (CYSNO), S-nitrosoglutathione (GSNO), S-nitroso-N-acetyl-D,L-penicillamine (SNAP) and hydroxylamine to that of nitric oxide (NO) and a vascular relaxing factor released by nerve stimulation in the guinea-pig intestine. The biological activity was examined in a bioassay system with guinea-pig colon as donor tissue and a series of spiral strips of rabbit aorta without endothelium as detector tissues. 2 Electrical stimulation of the guinea-pig colon released a vascular relaxing factor. The half-life of the relaxing factor down the bioassay cascade was the same as exogenously applied NO. N0-nitro-L-arginine (L-NOARG) inhibited the release of bioactivity. 3 The relaxations of the assay tissues caused by exogenous CYSNO also declined during the passage down the cascade. However, in the presence of L-cysteine (10-5 M) the half-life of CYSNO increased and there was no significant breakdown through the cascade. In contrast, the half-life of applied NO and the vascular relaxing factor released by nerve stimulation was unaffected by the presence of L-cysteine. 4 Exogenously applied GSNO (20-50 nM), SNAP (2-4 nM) and hydroxylamine (300-600 nM) caused relaxations that did not decline during the passage down the cascade. 5 In summary, the relaxation of the bioassay tissues during nerve stimulation was indistinguishable from the relaxation induced by NO, whereas relaxations induced by CYSNO, GSNO, SNAP and hydroxylamine showed different pharmacological profiles. The released bioactivity is thus likely to be NO itself.

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Colocalization of nitric oxide synthase and NADPH-diaphorase in the myenteric plexus of the rat gut

Cited by 197 publications

References 16 publications

A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice.

A novel pathogenesis of megacolon in Ncx/Hox11L.1 deficient mice.

Nitric oxide synthase in the enteric nervous system of the rainbow trout, Salmo gairdneri .

Smooth muscle relaxing effects of NO, nitrosothiols and a nerve‐induced relaxing factor released in guinea‐pig colon

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