100 research outputs found
The Microbiota-Gut-Brain Axis and Alzheimer Disease. From Dysbiosis to Neurodegeneration: Focus on the Central Nervous System Glial Cells
Get PDFGLP-2 receptor expression in excitatory and inhibitory enteric neurons and its role in mouse duodenum contractility.
Get PDFBackground. Glucagon-like peptide 2 (GLP-2), a nutrient-responsive hormone, exerts various actions in the gastrointestinal tract that are mediated by a G-protein
coupled receptor called GLP-2R. A little information is available on GLP-2R expression in enteric neurons and
nothing on the interstitial cells of Cajal (ICC). Methods. We investigated presence and distribution of the GLP-2R in the mouse duodenum by immunohistochemistry
and the potential motor effects of GLP-2 on
the spontaneous and neurally evoked mechanical activity. Key Results. The GLP-2R was expressed by the myenteric and submucosal neurons. Labelling was also
present in nerve varicosities within the circular muscular layer and at the deep muscular plexus (DMP). No immunoreactive nerve fiber was seen within the longitudinal
muscle layer. The GLP-2R-positive neurons
were either excitatory (SP- and choline-acetyltransferase-positive) or inhibitory (vasoactive intestinal polypeptide
and nNOS-positive). The ICC, both at the
myenteric plexus and at theDMP,never expressed GLP-2R but, especially those at the DMP, were surrounded by GLP-2R-positive nerve varicosities co-expressing either excitatory or inhibitory neurotransmitters.
Quantitative analysis demonstrated a consistent prevalence of GLP-2R on the excitatory pathways. In agreement, the functional results showed that the
administration of GLP-2 in vitro caused decrease of the spontaneous contractions mediated by nitric oxide release and reduction of the evoked cholinergic
contractions. Conclusions & Inferences. The present findings indicate that the GLP-2R is expressed by inhibitory and excitatory neurons, the GLP-2 inhibits the muscle contractility likely decreasing cholinergic
neurotransmission and increasing nitric oxide production, and this effect is possibly mediated by the ICC-DMP recruitment
Otilonium Bromide treatment prevents nitrergic functional and morphological changes caused by chronic stress in the distal colon of a rat IBS model
Get PDFIrritable bowel syndrome (IBS) is a highly prevalent gastrointestinal disorder characterized by periods of remission and exacerbation. Among the risk factors to develop IBS, psychosocial stress is widely acknowledged. The water avoidance stress repeatedly applied (rWAS) is considered effective to study IBS etio‐pathogenesis. Otilonium bromide (OB), a drug with multiple mechanisms of action, is largely used to treat IBS patients. Orally administered, it concentrates in the large bowel and significantly ameliorates the IBS symptomatology. Presently, we tested whether rWAS rats developed neuro‐muscular abnormalities in the distal colon and whether OB treatment prevented them. The investigation was focussed on the nitrergic neurotransmission by combining functional and morphological methodologies. The results confirm rWAS as reliable animal model to investigate the cellular mechanisms responsible for IBS: exposure to one‐hour psychosocial stress for 10 days depressed muscle contractility and increased iNOS expression in myenteric neurons. OB treatment counteracted these effects. We hypothesize that these effects are due to the corticotropin‐releasing factor (CRF) release, the main mediator of the psychosocial stress, followed by a CRF1receptor activation. OB, that was shown to prevent CRF1r activation, reasonably interrupted the cascade events that bring to the mechanical and immunohistochemical changes affecting rWAS rat colon
Complex patterns of chromosome 11 aberrations in myeloid malignancies target CBL, MLL, DDB1 and LMO2.
Get PDFNeurokinin receptors in the gastrointestinal muscle wall: cell distribution and possible roles.
No full textThe telocytes/myofibroblasts 3-D network forms a stretch receptor in the human bladder mucosa. Is this structure involved in the detrusor overactive diseases?
No full textThe Botulinum Treatment of Neurogenic Detrusor Overactivity: The Double-Face of the Neurotoxin.
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Human and mouse neurosphere transplantation regulate the function of aganglionic embryonic distal colon
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