Characterisation of neurons with nitric oxide synthase immunoreactivity that project to prevertebral ganglia

Anderson, C.R.; Furness, John B.; Woodman, Heather L.; Edwards, Scott A.; Crack, Peter J; Smith, A. Ian

doi:10.1016/0165-1838(94)00150-i

Cited by 88 publications

(39 citation statements)

References 25 publications

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“…Although NOS has been found in SPGNs projecting to other sympathetic targets (Blottner and Baumgarten, 1992;Dun et al, 1992;Saito et al, 1994;Anderson et al, 1995;Blottner et al, 1995), it was necessary to demonstrate that SPGNs projecting to IBAT contained NOS immunoreactivity. The NOS-ir neurons were restricted to the IML and central canal area of spinal cord, a distribution exactly matching that described by others (Blottner and Baumgarten, 1992;Dun et al, 1992;Saito et al, 1994;Anderson et al, 1995;Blottner et al, 1995). We examined horizontal sections of thoracic spinal cord of three animals that had been injected with the transneuronal retrograde marker PRV in IBAT.…”

Section: Vglut3-ir Terminals Synapse On Nos-ir Dendrites and Somata Imentioning

confidence: 99%

“…To determine whether the population of SPGNs projecting to sympathetic ganglia controlling IBAT were positive for NOS, a known marker of sympathetic preganglionic neurons (Blottner and Baumgarten, 1992;Dun et al, 1992;Saito et al, 1994;Anderson et al, 1995;Blottner et al, 1995), horizontal vibratome cut spinal cord sections were reacted for the simultaneous detection of NOS and PRV. Sections were first blocked with 10% horse serum in TBS and 0.1% Triton X-100 for 60 minutes.…”

Section: Light Microscopymentioning

confidence: 99%

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Coexpression of vesicular glutamate transporter‐3 and γ‐aminobutyric acidergic markers in rat rostral medullary raphe and intermediolateral cell column

Stornetta

Rosin

Simmons

et al. 2005

J of Comparative Neurology

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Markers of serotonergic, gamma-aminobutyric acid (GABA)-ergic (glutamic acid decarboxylase, 67 kDa isoform; GAD-67), and glutamatergic transmission (vesicular glutamate transporter 3; VGLUT3) have been detected in presumed sympathetic premotor neurons of the medullary raphe, a region that controls sympathetic tone to brown fat, skin blood vessels, and heart. In this study, the degree of coexpression of these markers was examined in raphe neurons by simultaneous histological detection of tryptophan hydroxylase (TrpOH) immunoreactivity with GAD-67 mRNA and VGLUT3 mRNA. Over half (52%) of the VGLUT3 mRNA-positive neurons expressed one or both of the other markers. The proportion of VGLUT3 neurons containing at least one of the other two markers was even higher (89%) for VGLUT3 spinally projecting neurons. VGLUT3 neurons containing markers for both serotonin and GABA were especially numerous (50-72%, depending on rostrocaudal level) within the marginal layer of raphe pallidus and the parapyramidal region. The dual GABAergic and glutamatergic nature of some bulbospinal raphe neurons was suggested by the presence of nerve terminals immunoreactive (ir) for both VGLUT3 and GABA in the intermediolateral cell column (IML) as detected by electron microscopy. VGLUT3-ir terminals formed approximately equal numbers of symmetric and asymmetric synapses onto presumed preganglionic neurons (nitric oxide synthase-ir profiles) or GABA-ir dendrites in IML, and terminals immunoreactive for both VGLUT3 and GABA always formed symmetric synapses. These data suggest that medullary raphe VGLUT3 neurons could inhibit sympathetic outflow and that their spinal targets include both preganglionic neurons and GABAergic interneurons.

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Section: Vglut3-ir Terminals Synapse On Nos-ir Dendrites and Somata Imentioning

confidence: 99%

Section: Light Microscopymentioning

confidence: 99%

Coexpression of vesicular glutamate transporter‐3 and γ‐aminobutyric acidergic markers in rat rostral medullary raphe and intermediolateral cell column

Stornetta

Rosin

Simmons

et al. 2005

J of Comparative Neurology

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“…The blood vessels were unpinned, washed in 0.01·mol·l -1 PBS (3ϫ10·min), incubated in DMSO (3ϫ10·min) and washed in 0.01·mol·l -1 PBS (5ϫ2·min). The blood vessels were then incubated in a polyclonal antibody raised against mouse endothelial NOS (1:1000) (O'Brien et al, 1995), or a polyclonal antibody raised against sheep neural NOS (1:4000) (Anderson et al, 1995), for 24·h at room temperature in a humid box. The following day, the tissues were washed in 0.01·mol·l -1 PBS (3ϫ10·min) to remove any excess antibody, and were incubated in a fluorescein isothiocyanate (FITC)-conjugated goat anti-mouse IgG or FITC-conjugated goat antisheep IgG (1:200) (Zymed Labratories, San Francisco, CA, USA) for 3-4·h at room temperature in a humid box.…”

Section: Endothelial and Neural Nos Immunohistochemistrymentioning

confidence: 99%

Dual mechanisms for nitric oxide control of large arteries in the estuarine crocodile Crocodylus porosus

Broughton

Donald

2007

Journal of Experimental Biology

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SUMMARY In reptiles, accumulating evidence suggests that nitric oxide (NO) induces a potent relaxation in the systemic vasculature. However, very few studies have examined the source from which NO is derived. Therefore, the present study used both anatomical and physiological approaches to establish whether NO-mediated vasodilation is via an endothelial or neural NO pathway in the large arteries of the estuarine crocodile Crocodylus porosus. Specific endothelial nitric oxide synthase (NOS) staining was observed in aortic endothelial cells following nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry and endothelial NOS immunohistochemistry (IHC), suggesting that an endothelial NO pathway is involved in vascular control. This finding was supported by in vitroorgan bath physiology, which demonstrated that the relaxation induced by acetylcholine (10-5 mol l-1) was abolished in the presence of the NOS inhibitor, N-omega-nitro-l-arginine(l-NNA; 10-4 mol l-1), the soluble guanylyl cyclase inhibitor, 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ;10-5 mol l-1), or when the endothelium was removed. Interestingly, evidence for a neural NO pathway was also identified in large arteries of the crocodile. Neural NOS was located in perivascular nerves of the major blood vessels following NADPH-d histochemistry and neural NOS IHC and in isolated aortic rings, l-NNA and ODQ, but not the removal of the endothelium, abolished the relaxation effect of the neural NOS agonist,nicotine (3×10-4 mol l-1). Thus, we conclude that the large arteries of C. porosus are potentially regulated by NO-derived from both endothelial and neural NOS.

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“…They were unpinned, washed in 0.01·mol·l -1 PBS (3×10·min), incubated in dimethyl sulphoxide (3×10·min) and washed in 0.01·mol·l -1 PBS (5×2·min). The vessels were then incubated in either sheep anti-neural NOS (1:4000; Anderson et al, 1995) or mouse anti-endothelial NOS (1:1000; O'Brien et al, 1995) for 24·h at room temperature in a humid box. The following day, tissues were washed in 0.01·mol·l -1 PBS (3×10·min) to remove any excess antibody and incubated in FITC-conjugated goat anti-sheep IgG (1:200) or FITC-conjugated goat anti-mouse IgG (1:200) (Zymed Laboratories, San Francisco, USA) for 3-4·h at room temperature in a humid box.…”

Section: Immunohistochemistrymentioning

confidence: 99%

Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis

Jennings

Broughton

Donald

2004

Journal of Experimental Biology

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of the endothelium. The nicotine-mediated dilation was blocked by the NOS inhibitor, N ω -nitro-L-arginine (L-NNA; 10 -4 ·mol·l -1 ), and ODQ (10 -5 ·mol·l -1 ). More specifically, the neural NOS inhibitor, N ω -propyl-Larginine (10 -5 ·mol·l -1 ), significantly decreased the dilation induced by nicotine (3×10 -4 ·mol·l -1 ). Furthermore, indomethacin (10 -5 ·mol·l -1 ) did not affect the nicotinemediated dilation, suggesting that prostaglandins are not involved in the response. Finally, the calcium ionophore A23187 (3×10 -6 ·mol·l -1 ) caused an endothelium-dependent dilation that was abolished in the presence of indomethacin. We propose the absence of an endothelial NO system in eel vasculature and suggest that neurally derived NO contributes to the maintenance of vascular tone in this species. In addition, we suggest that prostaglandins may act as endothelially derived relaxing factors in A. australis.

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Characterisation of neurons with nitric oxide synthase immunoreactivity that project to prevertebral ganglia

Cited by 88 publications

References 25 publications

Coexpression of vesicular glutamate transporter‐3 and γ‐aminobutyric acidergic markers in rat rostral medullary raphe and intermediolateral cell column

Coexpression of vesicular glutamate transporter‐3 and γ‐aminobutyric acidergic markers in rat rostral medullary raphe and intermediolateral cell column

Dual mechanisms for nitric oxide control of large arteries in the estuarine crocodile Crocodylus porosus

Nitric oxide control of the dorsal aorta and the intestinal vein of the Australian short-finned eel Anguilla australis

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