scholarly journals Chemically-Induced Inflammation Changes the Number of Nitrergic Nervous Structures in the Muscular Layer of the Porcine Descending Colon

Animals ◽  
2021 ◽  
Vol 11 (2) ◽  
pp. 394
Author(s):  
Liliana Rytel ◽  
Ignacy Gonkowski ◽  
Waldemar Grzegorzewski ◽  
Joanna Wojtkiewicz
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Pathological Condition ◽  
Nerve Fibers ◽  
Enteric Neurons ◽  
Muscular Layer ◽  
Gaseous Substance ◽  
Adaptive Processes ◽  
Experimental Inflammation ◽  
Descending Colon

The enteric nervous system (ENS) is the part of the nervous system that is located in the wall of the gastrointestinal tract and regulates the majority of the functions of the stomach and intestine. Enteric neurons may contain various active substances that act as neuromediators and/or neuromodulators. One of them is a gaseous substance, namely nitric oxide (NO). It is known that NO in the gastrointestinal (GI) tract may possess inhibitory functions; however, many of the aspects connected with the roles of this substance, especially during pathological states, remain not fully understood. An experiment is performed here with 15 pigs divided into 3 groups: C group (without any treatment), C1 group (“sham” operated), and C2 group, in which experimental inflammation was induced. The aim of this study is to investigate the influence of inflammation on nitrergic nervous structures in the muscular layer of the porcine descending colon using an immunofluorescence method. The obtained results show that inflammation causes an increase in the percentage of nitric oxide synthase (nNOS)-positive neurons in the myenteric plexus of the ENS, as well as the number of nitrergic nerve fibers in the muscular layer of the descending colon. The obtained results suggest that NO is involved in the pathological condition of the large bowel and probably takes part in neuroprotective and/or adaptive processes.

Student Research Award 1994: Nitric Oxide in the Rat Vestibular System

1994 ◽  
Vol 111 (4) ◽  
pp. 430-438 ◽  
Author(s):  
Andrew Harper ◽  
William R. Blythe ◽  
Carlton J. Zdanski ◽  
Jiri Prazma ◽  
Harold C. Pillsbury
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Amino Acid ◽  
Nitric Oxide Synthase ◽  
Vestibular System ◽  
Soluble Guanylate Cyclase ◽  
Excitatory Amino Acid ◽  
Nerve Fibers ◽  
Guanosine Monophosphate ◽  
Oxide Synthase

Nitric oxide is known to function as a neurotransmitter in the central nervous system. It is also known to be involved in the control nervous system excitatory amino acid neurotransmission cascade. Activation of excitatory amino acid receptors causes an influx of calcium, which activates nitric oxide synthase. The resulting increase in intracellular nitric oxide activates soluble guanylate cyclase, leading to a rise in cyclic guanosine monophosphate. The excitatory amino acids giutamate and aspartate are found in the vestibular system and have been postulated to function as vestibular system neurotransmitters. Although nitric oxide has ben investigated as a neurotransmitter in other tissues, no published studies have examined the role of nitric oxide in the vestibular system. Neuronal NADPH-dlaphorase has been characterized as a nitric oxide synthase. This enzyme catalyzes the conversion of L-arginine to l-citrulline, producing nitric oxide during the reaction. We used a histochemical stain characterized by Hope et al. (Proc Natl Acad Sci 1991;88:2811) as specific for neuronal nitric oxide synthase to localize the enzyme in the rat vestibular system. An Immunocytochemical stain was used to examine rat Inner ear tissue for the presence of the enzyme's end product, l-citrulline, thereby demonstrating nitric oxide synthase activity. Staining of vestibular ganglion sections showed nitric oxide synthase presence and activity in ganglion cells and nerve fibers. These results Indicate the presence of active nitric oxide synthase in these tissues and suggest modulation of vestibular neurotransmission by nitric oxide.

scholarly journals Hyperglycaemia-Induced Downregulation in Expression of nNOS Intramural Neurons of the Small Intestine in the Pig

2019 ◽  
Vol 20 (7) ◽  
pp. 1681 ◽  
Author(s):  
Michał Bulc ◽  
Katarzyna Palus ◽  
Michał Dąbrowski ◽  
Jarosław Całka
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Small Intestine ◽  
Enteric Nervous System ◽  
Molecular Mechanisms ◽  
Muscle Relaxation ◽  
Biologically Active ◽  
Enteric Neurons ◽  
Smooth Muscle Relaxation ◽  
Gi Tract

Diabetic autonomic peripheral neuropathy (PN) involves a broad spectrum of organs. One of them is the gastrointestinal (GI) tract. The molecular mechanisms underlying the pathogenesis of digestive complications are not yet fully understood. Digestion is controlled by the central nervous system (CNS) and the enteric nervous system (ENS) within the wall of the GI tract. Enteric neurons exert regulatory effects due to the many biologically active substances secreted and released by enteric nervous system (ENS) structures. These include nitric oxide (NO), produced by the neural nitric oxide synthase enzyme (nNOS). It is a very important inhibitory factor, necessary for smooth muscle relaxation. Moreover, it was noted that nitrergic innervation can undergo adaptive changes during pathological processes. Additionally, nitrergic neurons function may be regulated through the synthesis of other active neuropeptides. Therefore, in the present study, using the immunofluorescence technique, we first examined the influence of hyperglycemia on the NOS- containing neurons in the porcine small intestine and secondly the co-localization of nNOS with vasoactive intestinal polypeptide (VIP), galanin (GAL) and substance P (SP) in all plexuses studied. Following chronic hyperglycaemia, we observed a reduction in the number of the NOS-positive neurons in all intestinal segments studied, as well as an increased in investigated substances in nNOS positive neurons. This observation confirmed that diabetic hyperglycaemia can cause changes in the neurochemical characteristics of enteric neurons, which can lead to numerous disturbances in gastrointestinal tract functions. Moreover, can be the basis of an elaboration of these peptides analogues utilized as therapeutic agents in the treatment of GI complications.

Inflammation- and axotomy-induced changes in cocaine- and amphetamine-regulated transcript peptide-like immunoreactive (CART-LI) nervous structures in the porcine descending colon

2012 ◽  
Vol 15 (3) ◽  
pp. 517-524 ◽  
Author(s):  
P.J. Burliński
Keyword(s):  
Nervous System ◽  
Circular Muscle ◽  
Muscle Layer ◽  
Nerve Fibers ◽  
Immunofluorescence Technique ◽  
Physiological Conditions ◽  
Chemically Induced ◽  
Mucosal Layer ◽  
Descending Colon ◽  
Induced Changes

Abstract This study reports on changes in CART-like immunoreactive (CART-LI) nerve structures in the porcine descending colon during chemically driven inflammation and after axotomy. The distribution pattern of CART-LI nerve structures was studied using doublelabeling immunofluorescence technique in the circular muscle layer, myenteric (MP), outer submucous (OSP) and inner submucous plexuses (ISP) and also in the mucosal layer of the porcine descending colon in physiological conditions as well as under pathological factors. In the control animals, CART-LI perikarya have been shown to constitute 5.11% ± 0.64, 4.03% ± 1.17 and 0.05% ± 0.04 in MP, OSP and ISP, respectively. Changes in CART-immunoreactivity depended on the pathological factor and the part of the enteric nervous system (ENS) studied. Numbers of CART-LI perikarya amounted to 2.77% ± 0.64, 2.60% ± 0.36 and 0.26% ± 0.19 during chemically-induced colitis and 3.04% ± 0.88, 2.46% ± 0.8 and 0.43% ± 0.09 after axotomy in MP, OSP and ISP, respectively. Both studied pathological processes also caused an increase in the number of CART-LI nerve fibers in the circular muscle as well as in the mucosal layer.

Identification of cholinergic neurons in enteric nervous system by antibodies against choline acetyltransferase

1993 ◽  
Vol 265 (5) ◽  
pp. G1005-G1009 ◽  
Author(s):  
M. Schemann ◽  
H. Sann ◽  
C. Schaaf ◽  
M. Mader
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Choline Acetyltransferase ◽  
Polyclonal Antibodies ◽  
Neuronal Cell ◽  
Cholinergic Neurons ◽  
Nerve Fibers ◽  
Enteric Neurons ◽  
Cell Counts ◽  
Pelvic Ganglia

Several different monoclonal and polyclonal antibodies to choline acetyltransferase (ChAT) were screened to identify effective antibodies for immunocytochemical marking of cholinergic neurons in the enteric nervous system. Excellent immunohistochemical results were obtained with two of the antibodies in the myenteric plexus of the guinea pig stomach and small intestine. One was a mouse monoclonal antibody designated B3.9B3, and the second was a rabbit polyclonal antibody referred to as Peptide 3. Both antibodies clearly stained neuronal cell bodies as well as nerve fibers to the muscle layers and fibers encircling stained and unstained cell bodies. Cell counts indicated that approximately 64% (21.0 +/- 8.6 cells/ganglion) of gastric myenteric neurons are ChAT positive. Pelvic ganglia and the inferior mesenteric ganglia were examined as controls. Strong labeling of the majority of neurons was found in the pelvic ganglia, whereas few immunoreactive cells were apparent in the predominantly noradrenergic inferior mesenteric ganglion. Lack of effective antibodies to enteric neuronal ChAT has hampered progress in the study of the neurophysiology of cholinergic neurons in the digestive tract. Application of the B3.9B3 and Peptide 3 antibodies now promises to facilitate investigation of this important subset of enteric neurons.

Inhibitory effect of melatonin on nitric oxide synthase in rat enteric nervous system

2001 ◽  
Vol 120 (5) ◽  
pp. A176-A176
Author(s):  
P KOPPITZ ◽  
M STORR ◽  
D SAUR ◽  
M KURJAK ◽  
H ALLESCHER
Keyword(s):  
Nitric Oxide ◽  
Nervous System ◽  
Nitric Oxide Synthase ◽  
Enteric Nervous System ◽  
Inhibitory Effect ◽  
Oxide Synthase

scholarly journals Pathophysiological Roles of Neuro-Immune Interactions between Enteric Neurons and Mucosal Mast Cells in the Gut of Food Allergy Mice

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1586
Author(s):  
Tomoe Yashiro ◽  
Hanako Ogata ◽  
Syed Faisal Zaidi ◽  
Jaemin Lee ◽  
Shusaku Hayashi ◽  
...  
Keyword(s):  
Food Allergy ◽  
Mast Cells ◽  
Imaging System ◽  
Receptor Gene ◽  
Nerve Fibers ◽  
Enteric Neurons ◽  
Food Allergies ◽  
Adenosine A3 Receptor ◽  
Myenteric Neurons ◽  
Mucosal Mast Cells

Recently, the involvement of the nervous system in the pathology of allergic diseases has attracted increasing interest. However, the precise pathophysiological role of enteric neurons in food allergies has not been elucidated. We report the presence of functional high-affinity IgE receptors (FcεRIs) in enteric neurons. FcεRI immunoreactivities were observed in approximately 70% of cholinergic myenteric neurons from choline acetyltransferase-eGFP mice. Furthermore, stimulation by IgE-antigen elevated intracellular Ca2+ concentration in isolated myenteric neurons from normal mice, suggesting that FcεRIs are capable of activating myenteric neurons. Additionally, the morphological investigation revealed that the majority of mucosal mast cells were in close proximity to enteric nerve fibers in the colonic mucosa of food allergy mice. Next, using a newly developed coculture system of isolated myenteric neurons and mucosal-type bone-marrow-derived mast cells (mBMMCs) with a calcium imaging system, we demonstrated that the stimulation of isolated myenteric neurons by veratridine caused the activation of mBMMCs, which was suppressed by the adenosine A3 receptor antagonist MRE 3008F20. Moreover, the expression of the adenosine A3 receptor gene was detected in mBMMCs. Therefore, in conclusion, it is suggested that, through interaction with mucosal mast cells, IgE-antigen-activated myenteric neurons play a pathological role in further exacerbating the pathology of food allergy.

scholarly journals Age-related changes in nitric oxide activity, cyclic GMP, and TBARS levels in platelets and erythrocytes reflect the oxidative status in central nervous system

AGE ◽  
2012 ◽  
Vol 35 (2) ◽  
pp. 331-342 ◽  
Author(s):  
Elisa Mitiko Kawamoto ◽  
Andrea Rodrigues Vasconcelos ◽  
Sabrina Degaspari ◽  
Ana Elisa Böhmer ◽  
Cristoforo Scavone ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Central Nervous System ◽  
Nervous System ◽  
Cyclic Gmp ◽  
Oxidative Status ◽  
Age Related ◽  
Age Related Changes

Amitriptyline Neurotoxicity

2004 ◽  
Vol 100 (6) ◽  
pp. 1519-1525 ◽  
Author(s):  
Jean-Pierre Estebe ◽  
Robert R. Myers
Keyword(s):  
Nervous System ◽  
Sciatic Nerve ◽  
Local Anesthetic ◽  
Dose Range ◽  
Antidepressant Drug ◽  
Nerve Fibers ◽  
Anesthetic Agent ◽  
Sprague Dawley ◽  
Neurotoxic Effect ◽  
Local Anesthetic Agent

Background Amitriptyline is a tricyclic antidepressant drug used systemically for the management of neuropathic pain. Antidepressants, as a class of drugs with direct neurologic actions, are becoming widely used for the management of chronic pain, although their mechanisms are not entirely understood. Amitriptyline exerts potent effects on reuptake of norepinephrine and serotonin and blocks alpha 2A adrenoreceptors and N-methyl-D-aspartate receptors. Because amitriptyline is also a particularly potent blocker of sodium channels and voltage-gated potassium and calcium channels, it has been recommended as a long-acting local anesthetic agent. Unfortunately, amitriptyline has significant toxic side effects in the central nervous system and cardiovascular system that are dose-related to its systemic administration. Therefore, before amitriptyline can be used clinically as a local anesthetic agent, it should be thoroughly explored with respect to its direct neurotoxic effect in the peripheral nervous system. Methods The left sciatic nerve of Sprague-Dawley rats (12/ group) received a single topical amitriptyline dose of 0.625, 1.25, 2.5, or 5 mg; a saline group (n = 2) was used as control. Neuropathologic evaluations were conducted in separate animals (n = 4) 1, 3, and 7 days later. Results Amitriptyline topically applied in vivo to rat sciatic nerve causes a dose-related neurotoxic effect. Drug doses of 0.625-5 mg all caused Wallerian degeneration of peripheral nerve fibers, with the number of affected fibers and the severity of the injury directly related to the dose. Conclusion Because the effective local anesthetic dose is within this dose range, the authors strongly recommend that amitriptyline not be used as a local anesthetic agent.

scholarly journals Recent Advances in Biomarkers and Regenerative Medicine for Diabetic Neuropathy

2021 ◽  
Vol 22 (5) ◽  
pp. 2301
Author(s):  
Yoshikai Fujita ◽  
Tatsufumi Murakami ◽  
Akihiro Nakamura
Keyword(s):  
Diabetic Neuropathy ◽  
Target Gene ◽  
Pathological Condition ◽  
Nerve Fibers ◽  
Nerve Degeneration ◽  
Limb Amputation ◽  
Sensory Impairment ◽  
Mechanical Stimuli ◽  
Pathological Conditions ◽  
The Relationship

Diabetic neuropathy is one of the most common complications of diabetes. This complication is peripheral neuropathy with predominant sensory impairment, and its symptoms begin with hyperesthesia and pain and gradually become hypoesthesia with the loss of nerve fibers. In some cases, lower limb amputation occurs when hypoalgesia makes it impossible to be aware of trauma or mechanical stimuli. On the other hand, up to 50% of these complications are asymptomatic and tend to delay early detection. Therefore, sensitive and reliable biomarkers for diabetic neuropathy are needed for an early diagnosis of this condition. This review focuses on systemic biomarkers that may be useful at this time. It also describes research on the relationship between target gene polymorphisms and pathological conditions. Finally, we also introduce current information on regenerative therapy, which is expected to be a therapeutic approach when the pathological condition has progressed and nerve degeneration has been completed.

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