scholarly journals Distribution and colocalization of melatonin 1a-receptor and NADPH-d in the trigeminal system of rat

PeerJ ◽  
2019 ◽  
Vol 7 ◽  
pp. e6877 ◽  
Author(s):  
Yifan He ◽  
Wenguo Fan ◽  
Yue Xu ◽  
Yong liang Liu ◽  
Hongwen He ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Signal Processing ◽  
Distribution Pattern ◽  
Nicotinamide Adenine Dinucleotide ◽  
Sensory System ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Trigeminal System ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Melatonin 1A Receptor

Melatonin and nitric oxide (NO) are involved in orofacial signal processing in the trigeminal sensory system. The aim of the present study was to examine the distribution of melatonin 1a-receptor (MT1) and its colocalization with nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) in the spinal trigeminal nucleus (STN), the trigeminal ganglion (TG), and the mesencephalic trigeminal nucleus (MTN) in the rat, using histochemistry and immunohistochemistry. Our results show that MT1-positive neurons are widely distributed in the TG and the subnucleus caudalis of the STN. Furthermore, we found that MT1 colocalizes with NADPH-d throughout the TG and MTN, most extensively in the TG. The distribution pattern of MT1 and its colocalization with NADPH-d indicate that melatonin might play an important role in the trigeminal sensory system, which could be responsible for the regulation of NO levels.

scholarly journals Propofol Limits Microglial Activation after Experimental Brain Trauma through Inhibition of Nicotinamide Adenine Dinucleotide Phosphate Oxidase

2013 ◽  
Vol 119 (6) ◽  
pp. 1370-1388 ◽  
Author(s):  
Tao Luo ◽  
Junfang Wu ◽  
Shruti V. Kabadi ◽  
Boris Sabirzhanov ◽  
Kelsey Guanciale ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Reactive Oxygen Species ◽  
Nadph Oxidase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Microglial Activation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Interferon Γ ◽  
Oxygen Species ◽  
Neuroprotective Effects

Abstract Background: Microglial activation is implicated in delayed tissue damage after traumatic brain injury (TBI). Activation of microglia causes up-regulation of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, with the release of reactive oxygen species and cytotoxicity. Propofol appears to have antiinflammatory actions. The authors evaluated the neuroprotective effects of propofol after TBI and examined in vivo and in vitro whether such actions reflected modulation of NADPH oxidase. Methods: Adult male rats were subjected to moderate lateral fluid percussion TBI. Effect of propofol on brain microglial activation and functional recovery was assessed up to 28 days postinjury. By using primary microglial and BV2 cell cultures, the authors examined propofol modulation of lipopolysaccharide and interferon-γ–induced microglial reactivity and neurotoxicity. Results: Propofol improved cognitive recovery after TBI in novel object recognition test (48 ± 6% for propofol [n = 15] vs. 30 ± 4% for isoflurane [n = 14]; P = 0.005). The functional improvement with propofol was associated with limited microglial activation and decreased cortical lesion volume and neuronal loss. Propofol also attenuated lipopolysaccharide- and interferon-γ–induced microglial activation in vitro, with reduced expression of inducible nitric oxide synthase, nitric oxide, tumor necrosis factor-α, interlukin-1β, reactive oxygen species, and NADPH oxidase. Microglial-induced neurotoxicity in vitro was also markedly reduced by propofol. The protective effect of propofol was attenuated when the NADPH oxidase subunit p22phox was knocked down by small interfering RNA. Moreover, propofol reduced the expression of p22phox and gp91phox, two key components of NADPH oxidase, after TBI. Conclusion: The neuroprotective effects of propofol after TBI appear to be mediated, in part, through the inhibition of NADPH oxidase.

Nitric Oxide Synthase Is Deficient in the Aganglionic Colon of Patients With Hirschsprung's Disease

PEDIATRICS ◽  
1994 ◽  
Vol 93 (4) ◽  
pp. 647-651
Author(s):  
John F. Bealer ◽  
Eileen S. Natuzzi ◽  
Cori Buscher ◽  
Alan W. Flake ◽  
N. Scott Adzick ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Enzyme Activity ◽  
Smooth Muscle ◽  
Nitric Oxide Synthase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Hirschsprung's Disease ◽  
Hirschsprung’S Disease ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
No Synthase ◽  
Oxide Synthase

Objectives. The cause of Hirschsprung's disease is unknown but defects in nonadrenergic, noncholinergic innervation could prevent relaxation of aganglionic colon in patients with this disease. Nonadrenergic, noncholinergic nerves induce relaxation by using nitric oxide synthase to produce the smooth muscle relaxant nitric oxide (NO). In this study we asked whether aganglionic colon in patients with Hirschsprung's disease is deficient in NO synthase-containing nerves. Methodology. Using the tetrazolium blue dye method of demonstrating nicotinamide adenine dinucleotide phosphate-diaphorase enzymes, we examined eight colon specimens (four aganglionic and four ganglionic) from patients with Hirschsprung's disease for the presence of NO synthase. We further quantified NO synthase enzyme activity in these eight specimens by using the [3H]arginine-to-[3H]citrulline conversion assay. Results. The nicotinamide adenine dinucleotide phosphate-diaphorase staining showed that aganglionic colon contained less NO synthase than ganglionic colon. This NO synthase deficiency was located primarily in the nerves of the circular muscle layer of the colon. In addition, there was a striking difference in the NO synthase enzyme activity between aganglionic and ganglionic colon as measured by the [3H]arginine-to-[3H]citrulline conversion assay. Total NO synthase activity, as measured by this assay, was found to be less in aganglionic than in ganglionic colon. When the total activity was divided into its four known isoforms, aganglionic colon was noted to be striking deficient in the isoform derived primarily from nerves. Conclusion. We conclude that aganglionic colon is deficient in NO synthase-containing nerves. This deficiency could prevent smooth muscle relaxation in the aganglionic colon of patients with Hirschsprung's disease.

scholarly journals Putative antinociceptive action of nitric oxide in the caudal part of the spinal trigeminal nucleus during chronic carrageenan-induced arthritis in the rat temporomandibular joint

2009 ◽  
Vol 1302 ◽  
pp. 85-96 ◽  
Author(s):  
Silvia A. Tesser-Viscaíno ◽  
Alexandre Denadai-Souza ◽  
Simone A. Teixeira ◽  
Edílson Ervolino ◽  
Roelf J. Cruz-Rizzolo ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Temporomandibular Joint ◽  
Spinal Trigeminal Nucleus ◽  
Trigeminal Nucleus ◽  
Caudal Part ◽  
Antinociceptive Action

Acupuncture Increases Nitric Oxide Synthase Expression in Hippocampus of Streptozotocin-induced Diabetic Rats

2003 ◽  
Vol 31 (02) ◽  
pp. 305-313 ◽  
Author(s):  
Mi-Hyeon Jang ◽  
Min-Chul Shin ◽  
Baek-Vin Lim ◽  
Hyun-Bae Kim ◽  
Young-Pyo Kim ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Nicotinamide Adenine Dinucleotide ◽  
Acupuncture Treatment ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Diabetic Rats ◽  
Control Group ◽  
Diabetes Group ◽  
Zusanli Acupoint ◽  
Oxide Synthase

In the present study, the effect of acupuncture at Zusanli acupoint on nitric oxide synthase (NOS) expression in the hippocampus of streptozotocin (STZ)-induced diabetic rats was investigated via nicotinamide adenine dinucleotide phosphate-diaphorase (NADPH-d) histochemistry. Animals were divided into four groups: the control group, the nondiabetic and acupunctured group, the STZ-induced diabetes group, and the STZ-induced diabetes and acupunctured group. From the results, NADPH-d-positive neurons in the hippocampus were decreased in STZ-induced diabetic rats, while acupuncture increased NOS expression significantly under diabetic conditions. In the present study, it can be suggested that acupuncture treatment may modulate NOS activity in the hippocampus under diabetic conditions.

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