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Cholinergic Pathways (cholinergic + pathway)
Selected AbstractsThe otic ganglion in rats and its parotid connection: cholinergic pathways, reflex secretion and a secretory role for the facial nerveEXPERIMENTAL PHYSIOLOGY, Issue 1 2006Nina Khosravani Otic ganglionectomy in rats was found to have affected the parotid gland more profoundly than section of the auriculotemporal nerve as assesssed by reduction in gland weight (by 33 versus 20%) and total acetylcholine synthesizing capacity (by 88 versus 76%) 1 week postoperatively and, when assessed on the day of surgery under adrenoceptor blockade, by reflex secretion (by 99 versus 88%). The facial nerve contributed to the acetylcholine synthesizing capacity of the gland. Section of the nerve only, at the level of the stylomastoid foramen, reduced the acetylcholine synthesis by 15% and, combined with otic ganglionectomy, by 98% or, combined with section of the auriculotemporal nerve, by 82%. The facial nerve was secretory to the gland, and the response was of a cholinergic nature. The nerve conveyed reflex secretion of saliva and caused secretion of saliva upon stimulation. Most of the facial secretory nerve fibres originated from the otic ganglion, since after otic ganglionectomy (and allowing for nerve degeneration) the secretory response to facial nerve stimulation was markedly reduced (from 23 to 4 ,l (5 min),1). The persisting secetory response after otic ganglionectomy, exaggerated due to sensitization, and the residual acetylcholine synthesizing capacity (mainly depending on the facial nerve) showed that a minor proportion of pre- and postganglionic nerve fibres relay outside the otic ganglion. The great auricular nerve, which like the facial nerve penetrates the gland, caused no secretion of saliva upon stimulation. Avulsion of the auriculotemporal nerve was more effective than otic ganglionectomy in reducing the acetylcholine synthesizing capacity (by 94 versus 88%) and as effective as otic ganglionectomy in abolishing reflex secretion (by 99%). When aiming at parasympathetic denervation, avulsion may be the preferable choice, since it is technically easier to perform than otic ganglionectomy. [source] Cholinergic Mediation of Alcohol-Induced Experimental PancreatitisALCOHOLISM, Issue 10 2010Aurelia Lugea Objectives:, The mechanisms initiating pancreatitis in patients with chronic alcohol abuse are poorly understood. Although alcohol feeding has been previously suggested to alter cholinergic pathways, the effects of these cholinergic alterations in promoting pancreatitis have not been characterized. For this study, we determined the role of the cholinergic system in ethanol-induced sensitizing effects on cerulein pancreatitis. Methods:, Rats were pair-fed control and ethanol-containing Lieber-DeCarli diets for 6 weeks followed by parenteral administration of 4 hourly intraperitoneal injections of the cholecystokinin analog, cerulein at 0.5 ,g/kg. This dose of cerulein was selected because it caused pancreatic injury in ethanol-fed but not in control-fed rats. Pancreatitis was preceded by treatment with the muscarinic receptor antagonist atropine or by bilateral subdiaphragmatic vagotomy. Measurement of pancreatic pathology included serum lipase activity, pancreatic trypsin, and caspase-3 activities, and markers of pancreatic necrosis, apoptosis, and autophagy. In addition, we measured the effects of ethanol feeding on pancreatic acetylcholinesterase activity and pancreatic levels of the muscarinic acetylcholine receptors m1 and m3. Finally, we examined the synergistic effects of ethanol and carbachol on inducing acinar cell damage. Results:, We found that atropine blocked almost completely pancreatic pathology caused by cerulein administration in ethanol-fed rats, while vagotomy was less effective. Ethanol feeding did not alter expression levels of cholinergic muscarinic receptors in the pancreas but significantly decreased pancreatic acetylcholinesterase activity, suggesting that acetylcholine levels and cholinergic input within the pancreas can be higher in ethanol-fed rats. We further found that ethanol treatment of pancreatic acinar cells augmented pancreatic injury responses caused by the cholinergic agonist, carbachol. Conclusion:, These results demonstrate key roles for the cholinergic system in the mechanisms of alcoholic pancreatitis. [source] Octreotide enhances the accelerating effect of erythromycin on gastric emptying in healthy subjectsALIMENTARY PHARMACOLOGY & THERAPEUTICS, Issue 8 2002E. Athanasakis Summary Background : Erythromycin exhibits gastrokinetic properties through cholinergic pathways. Reports regarding the action of octreotide on gastric emptying are conflicting. Aim : To assess: (i) the hypothesis that serotonin receptors are involved in the accelerating effect of erythromycin on gastric emptying; and (ii) any modification of the gastrokinetic action of erythromycin induced by octreotide. Subjects and methods : Gastric emptying of a standard meal was estimated in 20 healthy subjects by scintigraphy on three different occasions in a double-blind, placebo-controlled manner and in random order: (i) after placebo; (ii) after 200 mg of intravenous erythromycin; and (iii) after 200 mg of intravenous erythromycin following pre-treatment with either 4 mg of intravenous ondansetron (10 subjects) or 50 µg octreotide. Results : Erythromycin significantly accelerated gastric emptying in all subjects by abolishing the lag phase. Pre-treatment with ondansetron abolished the accelerating effect of erythromycin by restoring the emptying times to placebo levels. Octreotide significantly enhanced the accelerating effect of erythromycin by reducing both the lag and post-lag phases of gastric emptying. Conclusions : Serotonin receptors are involved in the accelerating effect of erythromycin on gastric emptying. This effect seems to be enhanced by pre-treatment with octreotide, possibly as a result of the modification of the gastrointestinal hormonal environment. [source] The intestinal barrier and its regulation by neuroimmune factorsNEUROGASTROENTEROLOGY & MOTILITY, Issue 7 2010å. v. Keita Abstract Background, The ability to control uptake across the mucosa and protect from damage of harmful substances from the lumen is defined as intestinal barrier function. A disturbed barrier dysfunction has been described in many human diseases and animal models, for example, inflammatory bowel disease, irritable bowel syndrome, and intestinal hypersensitivity. In most diseases and models, alterations are seen both of the paracellular pathway, via the tight junctions, and of the transcellular routes, via different types of endocytosis. Recent studies of pathogenic mechanisms have demonstrated the important role of neuroimmune interaction with the epithelial cells in the regulation of barrier function. Neural impulses from extrinsic vagal and/or sympathetic efferent fibers or intrinsic enteric nerves influence mucosal barrier function via direct effects on epithelial cells or via interaction with immune cells. For example, by nerve-mediated activation by corticotropin-releasing hormone or cholinergic pathways, mucosal mast cells release a range of mediators with effects on transcellular, and/or paracellular permeability (for example, tryptase, TNF-,, nerve growth factor, and interleukins). Purpose, In this review, we discuss current physiological and pathophysiological aspects of the intestinal barrier and, in particular, its regulation by neuroimmune factors. [source] Propulsive activity induced by sequential electrical stimulation in the descending colon of the pigNEUROGASTROENTEROLOGY & MOTILITY, Issue 3 2005C. Sevcencu Abstract, This work was performed to study electrically induced contractions in the descending colon of pigs. Contractions were monitored using impedance planimetry and manometry. The luminal pressure, cross-sectional area (CSA), latency and velocity of CSA decrease were compared when using 3 ms, 9, 12, 15 or 30 mA pulses at 10 Hz for 10 s, and 15 mA, 0.03, 0.3 or 3 ms pulses at 10 Hz for 10 s. Stimulation was performed prior and after the application of N(G)-nitro- l - arginine methyl ester (l - NAME) and atropine. In the untreated colon, contraction was always of an ,off' type. A current increase from 9 to 30 mA increased the pressure. An increase of pulse duration from 0.03 to 3 ms shortened the latency, accelerated contraction and increased pressure. By sequential stimulation, contractions were coordinated to propel semi-fluid and solid luminal contents. l - NAME increased the magnitude of CSA decrease. Atropine induced inhibitory effects on contractions elicited by 3 ms pulses and abolished contractions induced by 0.03 and 0.3 ms pulses. In conclusion: (i) electrical stimulation evokes,off' colon contractions, which can be coordinated to result in propulsion; (ii) the best combination for current and pulse duration to induce propulsive contractions is 15 mA and 3 ms; (iii) nitrergic and cholinergic pathways mediate responses to electrical stimulation. [source] Nitrergic and cholinergic vagal pathways involved in the regulation of canine proximal gastric tone: an in vivo studyNEUROGASTROENTEROLOGY & MOTILITY, Issue 4 2000Paterson To better understand the relationship between cholinergic and nitrergic (NO) innervation in the regulation of proximal gastric (fundic) tone in vivo, the effects of nitric oxide synthase blockade on fundic tone were studied in conscious dogs using vagal cooling and an electronic barostat. Vagal cooling, atropine (0.05 mg kg,1 i.v. bolus) and hexamethonium (1 mg kg,1 i.v. bolus) all markedly decreased fundic tone as reflected by increased intragastric volume, indicating a significant contribution of vagal and enteric cholinergic pathways to the maintenance of canine fundic tone. Administration of L -NNA (10 mg kg,1 i.v. bolus) increased fundic tone and the effects of L -NNA were completely prevented by prior vagal cooling or atropine administration, but not by pretreatment with hexamethonium. The relaxation effects of neurally derived NO appear primarily related to inhibition of ongoing vagal cholinergic activity. The data are consistent with the primary site of action of nitrergic mechanisms on gastric fundic tone in conscious dogs being at a presynaptic site on vagal cholinergic efferent nerves. [source] | ||||||||||