Characterisation of cocaine- and amphetamine- regulated transcript-like immunoreactive (CART-LI) enteric neurons in the porcine small intestine

2012 ◽  
Vol 60 (3) ◽  
pp. 371-381 ◽  
Author(s):  
Joanna Wojtkiewicz ◽  
Sławomir Gonkowski ◽  
Marek Bladowski ◽  
Mariusz Majewski
Keyword(s):  
Nitric Oxide ◽  
Small Intestine ◽  
The Other ◽  
Enteric Neurons ◽  
Double Labelling ◽  
Immunofluorescence Technique ◽  
Submucous Plexus ◽  
Oxide Synthase ◽  
First Time ◽  
Labelling Immunofluorescence

The aim of this study was to investigate the distribution and the number of cocaine- and amphetamine-regulated transcript-like immunoreactive (CART-LI) neurons and the co-localisation of CART with substance P (SP), somatostatin (SOM), nitric oxide synthase (NOS) and vasoactive intestinal polypeptide (VIP) within the enteric nervous system (ENS) in the porcine small intestine. Accordingly, the myenteric plexus (MP), outer submucous plexus (OSP) and inner submucous plexus (ISP) of the small intestine (duodenum, jejunum and ileum) were studied by double-labelling immunofluorescence technique. CART-LI neurons were observed in all gut fragments and all types of intramural plexuses studied and amounted from 0.2 ± 0.1% in the ISP of ileum to 22.4 ± 2.4% in the MP of this segment. The co-localisation of CART and NOS or/and VIP was observed depending on the segment of the gut and the complexity of the intramural plexus. On the other hand, during this study the co-localisation of CART and SOM or/and SP was not observed. The present study, for the first time, presents a detailed description of the CART distribution pattern and co-localisation with other neuromodulators within the ENS of the porcine small intestine.

scholarly journals Neurochemical Plasticity of nNOS-, VIP- and CART-Immunoreactive Neurons Following Prolonged Acetylsalicylic Acid Supplementation in the Porcine Jejunum

2020 ◽  
Vol 21 (6) ◽  
pp. 2157
Author(s):  
Dominika Rząp ◽  
Marta Czajkowska ◽  
Jarosław Całka
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Acetylsalicylic Acid ◽  
Neuronal Plasticity ◽  
Adaptive Response ◽  
Neuronal Nitric Oxide Synthase ◽  
Double Labelling ◽  
Neurochemical Plasticity ◽  
Oxide Synthase ◽  
Labelling Immunofluorescence

Aspirin, also known as acetylsalicylic acid (ASA), is a commonly used anti-inflammatory drug that has analgesic and antipyretic properties. The side effects are well known, however, knowledge concerning its influence on gastric and intestinal innervation is limited. The enteric nervous system (ENS) innervates the whole gastrointestinal tract (GIT) and is comprised of more than one hundred million neurons. The capacity of neurons to adapt to microenvironmental influences, termed as an enteric neuronal plasticity, is an essential adaptive response to various pathological stimuli. Therefore, the goal of the present study was to determine the influence of prolonged ASA supplementation on the immunolocalization of neuronal nitric oxide synthase (nNOS), vasoactive intestinal peptide (VIP) and cocaine- and amphetamine- regulated transcript peptide (CART) in the porcine jejunum. The experiment was performed on 8 Pietrain × Duroc immature gilts. Using routine double-labelling immunofluorescence, we revealed that the ENS nerve cells underwent adaptive changes in response to the induced inflammation, which was manifested by upregulated or downregulated expression of the studied neurotransmitters. Our results suggest the participation of nNOS, VIP and CART in the development of inflammation and may form the basis for further neuro-gastroenterological research.

scholarly journals Proliferative enteropathy (PPE)-induced changes in the expression of DBH, VAChT and NOS in the neurons of intramural ganglia of the porcine ileum

2008 ◽  
Vol 53 (No. 10) ◽  
pp. 533-542 ◽  
Author(s):  
Z. Pidsudko ◽  
K. Wasowicz ◽  
J. Kaleczyc ◽  
M. Majewski ◽  
M. Lakomy
Keyword(s):  
Enteric Neurons ◽  
Double Labelling ◽  
Lawsonia Intracellularis ◽  
Large White ◽  
Submucous Plexus ◽  
Chemical Coding ◽  
Proliferative Enteropathy ◽  
Induced Changes ◽  
Oxide Synthase ◽  
Intramural Ganglia

As enteric neurons are regarded to be highly adaptive in their response to various pathological states, including inflammation, it appears to be of interest to study the chemical coding of neurons in the intramural ganglia of the ileum wall in the course of porcine proliferative enteropathy (PPE) evoked by <I>Lawsonia intracellularis.</I> The study was performed on 12 juvenile pigs of the Large White Polish breed. The pigs were divided into the control (C, <I>n</I> = 6) group and the group consisting of pigs with clinically diagnosed <I>Lawsonia intracellularis</I> infection (E, <I>n</I> = 6). In E group animals the infection was confirmed with a PCR-based test. All the animals were sacrificed and segments of the ileum being pathologically changed were processed for double-labelling immunofluorescence using antibody against protein gene-product 9.5 (PGP 9.5) combined with antibody for dopamine &beta;-hydroxylase (D&beta;H), vesicular acetylcholine transporter (VAChT) or nitric oxide synthase (NOS). Immunohistochemistry revealed in the inner submucous plexus (ISP) and outer submucous plexus (OSP) an increase of the number of neurons containing D&beta;H and VAChT in the E group. Interestingly, a decrease in the number of D&beta;H- and VAChT-positive neurons in meynteric plexus (MP) ganglia of the E group animals was observed. The most remarkable difference in the chemical coding of enteric neurons between the control and PPE-suffering pigs was a significant increase of the number of NOS-positive nerve cells in the MP and OSP of the infected animals. The present results show that acetylcholine, catecholamines and NO may be involved in the regulation of functions of the porcine enteric nerve pathways not only under physiological, but also pathological conditions.

CO2 laser enhances the chilling tolerance of wheat seedlings by stimulating NO synthesis

2016 ◽  
Vol 96 (5) ◽  
pp. 796-807
Author(s):  
Yi-ping Chen ◽  
Qiang Liu ◽  
Dong Chen
Keyword(s):  
Nitric Oxide ◽  
Laser Irradiation ◽  
Sodium Tungstate ◽  
Chilling Stress ◽  
Chilling Tolerance ◽  
The Other ◽  
Control Group ◽  
Wheat Seedlings ◽  
Oxide Synthase ◽  
Protein Treatment

To investigate the mechanism by which laser irradiation enhances the chilling tolerance of wheat seedlings, seeds were exposed to different treatments, and biochemical parameters were measured. Compared with the control group, chilling stress (CS) led to an increase in the concentrations of malondialdehyde (MDA) and H2O2, and decreases in the activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), glutathione reductase (GR), catalase (CAT), peroxidase (POD), and nitric oxide synthase (NOS), and the concentrations of nitric oxide (NO) and protein. Treatment with 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide (PTIO), sodium tungstate (ST), and NG-nitro-L-arginine methyl ester (L-NAME) followed by CS resulted in further increases in the concentrations of MDA and H2O2 and further decreases in the other parameters. However, treatment with PTIO, ST, and L-NAME followed by laser irradiation had the opposite effects on these parameters. When the seeds were treated with PTIO, ST, and L-NAME followed by laser and CS, the concentrations of MDA and H2O2 were significantly lower and the other parameters were higher than in the PTIO, ST, and L-NAME plus CS groups. These results suggest that CO2 laser irradiation enhances the chilling tolerance of wheat seedlings by stimulating endogenous NO synthesis.

Increasing dihydrobiopterin causes dysfunction of endothelial nitric oxide synthase in rats in vivo

2011 ◽  
Vol 301 (3) ◽  
pp. H721-H729 ◽  
Author(s):  
Katsuhiko Noguchi ◽  
Naobumi Hamadate ◽  
Toshihiro Matsuzaki ◽  
Mayuko Sakanashi ◽  
Junko Nakasone ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Endothelial Nitric Oxide Synthase ◽  
Control Treatment ◽  
Enos Uncoupling ◽  
Nos Inhibitor ◽  
Oxide Synthase ◽  
Endothelial Nitric Oxide ◽  
First Time

An elevation of oxidized forms of tetrahydrobiopterin (BH4), especially dihydrobiopterin (BH2), has been reported in the setting of oxidative stress, such as arteriosclerotic/atherosclerotic disorders, where endothelial nitric oxide synthase (eNOS) is dysfunctional, but the role of BH2 in the regulation of eNOS activity in vivo remains to be evaluated. This study was designed to clarify whether increasing BH2 concentration causes endothelial dysfunction in rats. To increase vascular BH2 levels, the BH2 precursor sepiapterin (SEP) was intravenously given after the administration of the specific dihydrofolate reductase inhibitor methotrexate (MTX) to block intracellular conversion of BH2 to BH4. MTX/SEP treatment did not significantly affect aortic BH4 levels compared with control treatment. However, MTX/SEP treatment markedly augmented aortic BH2 levels (291.1 ± 29.2 vs. 33.4 ± 6.4 pmol/g, P < 0.01) in association with moderate hypertension. Treatment with MTX alone did not significantly alter blood pressure or BH4 levels but decreased the BH4-to-BH2 ratio. Treatment with MTX/SEP, but not with MTX alone, impaired ACh-induced vasodilator and depressor responses compared with the control treatment (both P < 0.05) and also aggravated ACh-induced endothelium-dependent relaxations ( P < 0.05) of isolated aortas without affecting sodium nitroprusside-induced endothelium-independent relaxations. Importantly, MTX/SEP treatment significantly enhanced aortic superoxide production, which was diminished by NOS inhibitor treatment, and the impaired ACh-induced relaxations were reversed with SOD ( P < 0.05), suggesting the involvement of eNOS uncoupling. These results indicate, for the first time, that increasing BH2 causes eNOS dysfunction in vivo even in the absence of BH4 deficiency, demonstrating a novel insight into the regulation of endothelial function.

NO nerves in a tapeworm. NADPH-diaphorase histochemistry in adult Hymenolepis diminuta

Parasitology ◽  
1996 ◽  
Vol 113 (6) ◽  
pp. 559-565 ◽  
Author(s):  
M. K. S. Gustafsson ◽  
A. M. Lindholm ◽  
N. B. Terenina ◽  
M. Reuter
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nadph Diaphorase ◽  
Hymenolepis Diminuta ◽  
Staining Reaction ◽  
Internal Seminal Vesicle ◽  
Oxide Synthase ◽  
First Time ◽  
The Brain ◽  
Nerve Cords

SUMMARYThe free radical nitric oxide (NO), which is synthesized by nitric oxide synthase (NOS), has recently been discovered to function as a neuronal messenger. The presence of NOS was detected in the nervous system of adult Hymenolepis diminuta with NADPH-diaphorase (NADPH-d) histochemistry. The NADPH-d histochemical reaction is regarded as a selective marker for NOS in neuronal tissue. NADPH-d staining was observed in nerve fibres in the main and minor nerve cords and the transverse ring commissures, and in cell bodies in the brain commissure, along the main nerve cords, in the suckers and the rostellar sac. NADPH-d staining was also observed in the wall of the internal seminal vesicle and the genital atrium. The pattern of NADPH-d staining was compared with that of the 5-HT immunoreactive nervous elements. The NADPH-d staining reaction and the 5-HT immunoreactivity occur in separate sets of neurons. This is the first time the NADPH-d reaction has been demonstrated in the nervous system of a flatworm, indicating that NOS is present and that NO can be produced at this level of evolution.

Abstract 18060: TRAIL Promotes Angiogenesis and Ischemia-Induced Neovascularisation via NOX4, H2O2 and Nitric Oxide-Dependent Mechanisms

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Belinda A Di Bartolo ◽  
Sian P Cartland ◽  
Leonel Prado-Lourenco ◽  
Nor Saadah M Azahri ◽  
Thuan Thai ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Angiogenic Factor ◽  
Tubule Formation ◽  
Nitric Oxide Synthase Inhibitor ◽  
Therapeutic Implications ◽  
Synthase Inhibitor ◽  
Oxide Synthase ◽  
First Time

Background: Angiogenesis and neovascularization are essential processes that follow ischemia insults. Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) not only induces endothelial cell (EC) death and inhibits angiogenesis, but also promotes EC migration, invasion and proliferation in vitro . These seemingly opposite effects make its role in angiogenesis in vivo unclear. Using TRAIL -/- and wild-type mice, we sought to determine the role of TRAIL in angiogenesis and neovascularisation. We also sought mechanisms in vitro . Methods and Results: Reduced vascularisation assessed by real-time in vivo 3D Vevo ultrasound imaging and CD31 staining was observed in TRAIL -/- mice 28 d after hindlimb ischemia. Moreover, reduced capillary formation and increased apoptosis was evident in TRAIL -/- muscles even at 3 d after ischemic surgery. We have previously shown that fibroblast growth factor-2 (FGF-2), a potent angiogenic factor, regulates TRAIL gene expression in vascular smooth muscle cells. Indeed, FGF-2 also regulates TRAIL expression in ECs, and FGF-2-inducible proliferation, migration and tubule formation was inhibited with siRNA targeting TRAIL. Notably, both FGF-2 and TRAIL significantly increased NOX4 expression. TRAIL-inducible angiogenic activity in ECs was inhibited with siRNAs targeting NOX4, and consistent with these, NOX4 mRNA was reduced in 3 d ischemic hindlimbs of TRAIL -/- mice. TRAIL stimulated intracellular H 2 O 2 levels in ECs, and TRAIL-inducible proliferation, migration and tubule formation was inhibited with not only PEG-catalase, a H 2 O 2 scavenger, but also blocked with L-NAME, a nitric oxide synthase inhibitor. Conclusions: This is the first demonstration showing that TRAIL promotes angiogenesis in vivo . We show for the first time that the TRAIL stimulates NOX4 expression to mediate nitric oxide-dependent angiogenic effects. This has significant therapeutic implications such that TRAIL may improve the angiogenic response to ischemia and increase perfusion recovery in patients with CVD and diabetes.

scholarly journals The T2 Toxin Produced by Fusarium spp. Impacts Porcine Duodenal Nitric Oxide Synthase (nNOS)-Positive Nervous Structures—The Preliminary Study

2020 ◽  
Vol 21 (14) ◽  
pp. 5118
Author(s):  
Andrzej Rychlik ◽  
Slawomir Gonkowski ◽  
Ewa Kaczmar ◽  
Kazimierz Obremski ◽  
Jaroslaw Calka ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Enteric Neurons ◽  
Fusarium Spp ◽  
Internal Organs ◽  
Preliminary Study ◽  
Living Organisms ◽  
T2 Toxin ◽  
Oxide Synthase

T2 toxin synthetized by Fusarium spp. negatively affects various internal organs and systems, including the digestive tract and the immune, endocrine, and nervous systems. However, knowledge about the effects of T2 on the enteric nervous system (ENS) is still incomplete. Therefore, during the present experiment, the influence of T2 toxin with a dose of 12 µg/kg body weight (b.w.)/per day on the number of enteric nervous structures immunoreactive to neuronal isoform nitric oxide synthase (nNOS—used here as a marker of nitrergic neurons) in the porcine duodenum was studied using the double immunofluorescence method. Under physiological conditions, nNOS-positive neurons amounted to 38.28 ± 1.147%, 38.39 ± 1.244%, and 35.34 ± 1.151 of all enteric neurons in the myenteric (MP), outer submucous (OSP), and inner submucous (ISP) plexuses, respectively. After administration of T2 toxin, an increase in the number of these neurons was observed in all types of the enteric plexuses and nNOS-positive cells reached 46.20 ± 1.453% in the MP, 45.39 ± 0.488% in the OSP, and 44.07 ± 0.308% in the ISP. However, in the present study, the influence of T2 toxin on the intramucosal and intramuscular nNOS-positive nerves was not observed. The results obtained in the present study indicate that even low doses of T2 toxin are not neutral for living organisms because they may change the neurochemical characterization of the enteric neurons.

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