Nitric oxide-induced oxidative stress impairs pacemaker function of murine interstitial cells of Cajal during inflammation

2016 ◽  
Vol 111 ◽  
pp. 838-848 ◽  
Author(s):  
Noriyuki Kaji ◽  
Kazuhide Horiguchi ◽  
Satoshi Iino ◽  
Shinsuke Nakayama ◽  
Tomohiko Ohwada ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Pacemaker Function ◽  
Cells Of Cajal

Regulation of interstitial cells of Cajal in the mouse gastric body by neuronal nitric oxide

2007 ◽  
Vol 19 (7) ◽  
pp. 585-595 ◽  
Author(s):  
k. m. choi ◽  
s. j. gibbons ◽  
j. l. roeder ◽  
m. s. lurken ◽  
j. zhu ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interstitial Cells Of Cajal ◽  
Interstitial Cells ◽  
Gastric Body ◽  
Cells Of Cajal

scholarly journals Enteric neuronal plasticity and a reduced number of interstitial cells of Cajal in hypertrophic rat ileum

Gut ◽  
1998 ◽  
Vol 42 (6) ◽  
pp. 836-844 ◽  
Author(s):  
E Ekblad ◽  
R Sjuve ◽  
A Arner ◽  
F Sundler
Keyword(s):  
Nitric Oxide ◽  
Nitric Oxide Synthase ◽  
Interstitial Cells Of Cajal ◽  
In Situ Hybridisation ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Work Load ◽  
Interstitial Cells ◽  
Nadph Diaphorase ◽  
Cells Of Cajal ◽  
Oxide Synthase

Background—Partial obstruction of the ileum causes a notable hypertrophy of smooth muscle cells and enteric neurones in the proximally located intestine.Aims—To study the expression of neuromessengers in the hypertrophic ileum of rat as little is known about neuromessenger plasticity under these conditions. To investigate the presence of interstitial cells of Cajal (ICC) in hypertrophic ileum.Methods—Ileal hypertrophy was induced by circumferential application of a strip of plastic film for 18–24 days. Immunocytochemistry, in situ hybridisation, nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry, and ethidium bromide staining were used to investigate the number of enteric neurones expressing neuropeptides and nitric oxide synthase, and the frequency of ICC.Results—In the hypertrophic ileum several neuronal populations showed changes in their expression of neuromessengers. Myenteric neurones expressing vasoactive intestinal peptide (VIP), pituitary adenylate cyclase activating peptide, and galanin were notably increased in number. In submucous ganglia the number of VIP immunoreactive neurones decreased while those expressing VIP mRNA increased. NADPH diaphorase positive submucous neurones increased dramatically while the number of neuronal type nitric oxide synthase expressing ones was unchanged. The number of ICC decreased notably in hypertrophic ileum.Conclusion—Enteric neurones change their levels of expression of neuromessengers in hypertrophic ileum. ICC are also affected. The changes are presumably part of an adaptive response to the increased work load.

scholarly journals Loss of nitric oxide-mediated inhibition of purine neurotransmitter release in the colon in the absence of interstitial cells of Cajal

2017 ◽  
Vol 313 (5) ◽  
pp. G419-G433 ◽  
Author(s):  
Leonie Durnin ◽  
Andrea Lees ◽  
Sheerien Manzoor ◽  
Kent C. Sasse ◽  
Kenton M. Sanders ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Interstitial Cells Of Cajal ◽  
Colonic Motility ◽  
Circular Muscle ◽  
Electrical Field Stimulation ◽  
Interstitial Cells ◽  
Partial Loss ◽  
Purinergic Neurotransmission ◽  
Cells Of Cajal

Regulation of colonic motility depends on the integrity of enteric inhibitory neurotransmission mediated by nitric oxide (NO), purine neurotransmitters, and neuropeptides. Intramuscular interstitial cells of Cajal (ICC-IM) and platelet-derived growth factor receptor-α-positive (PDGFRα+) cells are involved in generating responses to NO and purine neurotransmitters, respectively. Previous studies have suggested a decreased nitrergic and increased purinergic neurotransmission in KitW/KitW-v ( W/Wv) mice that display lesions in ICC-IM along the gastrointestinal tract. However, contributions of NO to these phenotypes have not been evaluated. We used small-chamber superfusion assays and HPLC to measure the spontaneous and electrical field stimulation (EFS)-evoked release of nicotinamide adenine dinucleotide (NAD+)/ADP-ribose, uridine adenosine tetraphosphate (Up4A), adenosine 5′-triphosphate (ATP), and metabolites from the tunica muscularis of human, monkey, and murine colons and circular muscle of monkey colon, and we tested drugs that modulate NO levels or blocked NO receptors. NO inhibited EFS-evoked release of purines in the colon via presynaptic neuromodulation. Colons from W/Wv, Nos1−/−, and Prkg1−/− mice displayed augmented neural release of purines that was likely due to altered nitrergic neuromodulation. Colons from W/Wv mice demonstrated decreased nitrergic and increased purinergic relaxations in response to nerve stimulation. W/Wv mouse colons demonstrated reduced Nos1 expression and reduced NO release. Our results suggest that enhanced purinergic neurotransmission may compensate for the loss of nitrergic neurotransmission in muscles with partial loss of ICC. The interactions between nitrergic and purinergic neurotransmission in the colon provide novel insight into the role of neurotransmitters and effector cells in the neural regulation of gastrointestinal motility. NEW & NOTEWORTHY This is the first study investigating the role of nitric oxide (NO) and intramuscular interstitial cells of Cajal (ICC-IM) in modulating neural release of purines in colon. We found that NO inhibited release of purines in human, monkey, and murine colons and that colons from KitW/KitW-v ( W/Wv) mice, which present with partial loss of ICC-IM, demonstrated augmented neural release of purines. Interactions between nitrergic and purinergic neurotransmission may affect motility in disease conditions with ICC-IM deficiencies.

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