Neurochemical phenotype and function of endomorphin-2-containing neurons in the myenteric plexus of the rat colon

2010 ◽  
Vol 34 (8) ◽  
pp. S19-S19
Author(s):  
Jun‑Ping Li ◽  
Chang‑Jun Gao ◽  
Bo‑Chang Lü ◽  
Ting Zhang ◽  
Jiang‑Bo Ma ◽  
...  
Keyword(s):  
Myenteric Plexus ◽  
Rat Colon ◽  
And Function

scholarly journals Neurochemical phenotype and function of endomorphin 2-immunopositive neurons in the myenteric plexus of the rat colon

2014 ◽  
Vol 8 ◽  
Author(s):  
Jun-Ping Li ◽  
Xi-Yu Wang ◽  
Chang-Jun Gao ◽  
Yong-Hui Liao ◽  
Juan Qu ◽  
...  
Keyword(s):  
Myenteric Plexus ◽  
Rat Colon ◽  
And Function

scholarly journals A novel nutrient sensing mechanism underlies substrate-induced regulation of monocarboxylate transporter-1

2012 ◽  
Vol 303 (10) ◽  
pp. G1126-G1133 ◽  
Author(s):  
Alip Borthakur ◽  
Shubha Priyamvada ◽  
Anoop Kumar ◽  
Arivarasu A. Natarajan ◽  
Ravinder K. Gill ◽  
...  
Keyword(s):  
Intestinal Inflammation ◽  
Apical Membrane ◽  
Nutrient Sensing ◽  
Monocarboxylate Transporter ◽  
Rat Colon ◽  
Intracellular Camp ◽  
Short Term ◽  
Monocarboxylate Transporter 1 ◽  
Sensing Mechanism ◽  
And Function

Monocarboxylate transporter isoform-1 (MCT1) plays an important role in the absorption of short-chain fatty acids (SCFAs) in the colon. Butyrate, a major SCFA, serves as the primary energy source for the colonic mucosa, maintains epithelial integrity, and ameliorates intestinal inflammation. Previous studies have shown substrate (butyrate)-induced upregulation of MCT1 expression and function via transcriptional mechanisms. The present studies provide evidence that short-term MCT1 regulation by substrates could be mediated via a novel nutrient sensing mechanism. Short-term regulation of MCT1 by butyrate was examined in vitro in human intestinal C2BBe1 and rat intestinal IEC-6 cells and ex vivo in rat intestinal mucosa. Effects of pectin feeding on MCT1, in vivo, were determined in rat model. Butyrate treatment (30–120 min) of C2BBe1 cells increased MCT1 function {p-(chloromercuri) benzene sulfonate (PCMBS)-sensitive [14C]butyrate uptake} in a pertussis toxin-sensitive manner. The effects were associated with decreased intracellular cAMP levels, increased Vmax of butyrate uptake, and GPR109A-dependent increase in apical membrane MCT1 level. Nicotinic acid, an agonist for the SCFA receptor GPR109A, also increased MCT1 function and decreased intracellular cAMP. Pectin feeding increased apical membrane MCT1 levels and nicotinate-induced transepithelial butyrate flux in rat colon. Our data provide strong evidence for substrate-induced enhancement of MCT1 surface expression and function via a novel nutrient sensing mechanism involving GPR109A as a SCFA sensor.

Distribution and function of enteric GAL-IR nerves in dogs: comparison with VIP

1989 ◽  
Vol 256 (5) ◽  
pp. G884-G896 ◽  
Author(s):  
T. Gonda ◽  
E. E. Daniel ◽  
T. J. McDonald ◽  
J. E. Fox ◽  
B. D. Brooks ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Small Intestine ◽  
Gastrointestinal Tract ◽  
Vasoactive Intestinal Polypeptide ◽  
Myenteric Plexus ◽  
Low Doses ◽  
Field Stimulation ◽  
And Function ◽  
Higher Doses ◽  
Stimulation Of

The distribution of nerves containing galanin-immunoreactive (GAL-IR) material was compared to the distribution of neurons containing vasoactive intestinal polypeptide (VIP) immunoreactivity in the canine gastrointestinal tract. The actions of intra-arterially administered galanin and VIP on motility in the gastric antrum and corpus and the intestines were also studied. All sphincter muscles contained galanin- and VIP-immunoreactive nerve profiles. VIP-immunoreactive nerve profiles were present in all layers of the stomach, small intestine, and colon. GAL-IR nerve somata were common in the submucous plexus of ileum and colon and in the myenteric plexus of the terminal antrum, as were nerve processes in various layers. In the small intestine, galanin inhibited contractile responses to field stimulation of intrinsic nerves and also reduced the contractions after nerve blockade with tetrodotoxin (TTX). VIP often enhanced field-stimulated contractions at low doses but inhibited these and the contractions after TTX at higher doses. In the stomach and colon, both peptides inhibited responses to field stimulation; whether these effects were due to actions on smooth muscle was not tested. The distribution and actions of galanin in gut are consistent with the hypothesis that it acts at smooth muscle sites and possibly at prejunctional sites.

Urocortin I is present in the enteric nervous system and exerts an excitatory effect via cholinergic and serotonergic pathways in the rat colon

2007 ◽  
Vol 293 (4) ◽  
pp. G903-G910 ◽  
Author(s):  
Takazumi Kimura ◽  
Tomofumi Amano ◽  
Hirotsugu Uehara ◽  
Hajime Ariga ◽  
Tsuyoshi Ishida ◽  
...  
Keyword(s):  
Nervous System ◽  
Enteric Nervous System ◽  
Motor Function ◽  
Myenteric Plexus ◽  
Neuronal Cells ◽  
Colonic Transit ◽  
Rat Colon ◽  
Excitatory Effect ◽  
Potent Effect ◽  
Colonic Motor

Corticotropin-releasing factor (CRF) and urocortin I (UcnI) have been shown to accelerate colonic transit after central nervous system (CNS) or peripheral administration, but the mechanism of their peripheral effect on colonic motor function has not been fully investigated. Furthermore, the localization of UcnI in the enteric nervous system (ENS) of the colon is unknown. We investigated the effect of CRF and UcnI on colonic motor function and examined the localization of CRF, UcnI, CRF receptors, choline acetyltransferase (ChAT), and 5-HT. Isometric tension of rat colonic muscle strips was measured. The effect of CRF, UcnI on phasic contractions, and electrical field stimulation (EFS)-induced off-contractions were examined. The effects of UcnI on both types of contraction were also studied in the presence of antalarmin, astressin2-B, tetrodotoxin (TTX), atropine, and 5-HT antagonists. The localizations of CRF, UcnI, CRF receptors, ChAT, and 5-HT in the colon were investigated by immunohistochemistry. CRF and UcnI increased both contractions dose dependently. UcnI exerted a more potent effect than CRF. Antalarmin, TTX, atropine, and 5-HT antagonists abolished the contractile effects of UcnI. CRF and UcnI were observed in the neuronal cells of the myenteric plexus. UcnI and ChAT, as well as UcnI and 5-HT, were colocalized in some of the neuronal cells of the myenteric plexus. This study demonstrated that CRF and UcnI act on the ENS and increase colonic contractility by enhancing cholinergic and serotonergic neurotransmission. These peptides are present in myenteric neurons. CRF and, perhaps, to a greater extent, UcnI appear to act as neuromodulators in the ENS of the rat colon.

The myenteric plexus of the rat colon after fecal stream diversion: a morpho-quantitative study

2004 ◽  
Vol 114 (1-2) ◽  
pp. 39-46 ◽  
Author(s):  
Ricardo Braganca de Vasconcellos Fontes ◽  
Luis Bernardo Froes ◽  
Erick Dancuart Omar ◽  
Edson Aparecido Liberti
Keyword(s):  
Quantitative Study ◽  
Myenteric Plexus ◽  
Rat Colon ◽  
Fecal Stream

Localization and function of adenosine receptor subtypes at the longitudinal muscle – Myenteric plexus of the rat ileum

2011 ◽  
Vol 59 (7) ◽  
pp. 1043-1055 ◽  
Author(s):  
Cátia Vieira ◽  
Fátima Ferreirinha ◽  
Isabel Silva ◽  
Margarida Duarte-Araújo ◽  
Paulo Correia-de-Sá
Keyword(s):  
Adenosine Receptor ◽  
Myenteric Plexus ◽  
Longitudinal Muscle ◽  
Receptor Subtypes ◽  
Rat Ileum ◽  
And Function
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