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Acetylcholine - Crossref

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Last Updated: 10 November 2022

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ACETYLCHOLINE AND ITS SYNTHESIZING ENZYME CHOLINE ACETYLTRANSPHERASE IN THE ENTERIC NERVOUS SYSTEM

The enteric nervous system is the most extensive and costly segment of the peripheral nervous system. Three major classes of neurons in the enteric nervous system—u2013 primary afferent, interneurons, and motor neurons — are described in neurochemical, pharmacological, and functional experiments. Acetylcholine is the primary excitatory neurotransmitter in the enteric nervous system, controlling motility and mucosal function in the digestive system, according to internal cholinergic neurons and vagus terminals. The ChAT mRNA splicing variants of ChAT mRNA that are transcribed from the ChAT gene are the splicing variants of ChAT mRNA that are transcribed from the ChAT gene. The splicing variants of ChAT mRNA are the splicing variants of ChAT mRNA that are transcribed from the ChAT gene, according to the latest markers used to analyze cholinergic structures. ChAT mRNA variants are transcribed in several animal species, including humans, in various animal species, such as humans. Morphological, genetic, and molecular analysis of ChAT and its splicing variants, as the most reliable and commonly used marker for cholinergic pathways in the enteric nervous system, may lead to a better understanding of the physiological and pathological properties of cholinergic neurons.

Source link: https://doi.org/10.5272/jimab.2022284.4671


Autonomic nerve dysfunction in COPD as assessed by the acetylcholine sweat-spot test

Patients with hypoxic chronic pulmonary disease have signs of a subsympathetic autonomic neuropathy, with apparent preservation of sympathetic function. This sweat gland test assesses sympathetic nerve function, because it depends on the fact that denervated sweat glands do not produce sweat. Thirty patients with hypoxaemic COPD and seven age matched normal subjects were studied. In eight COPD patients, the acetylcholine sweat-spot test was highly reproducible, with no individual with a normal or otherwise exceptional function being incorrectly assigned. The age control subjects were found to have normal acetylcholine sweat-spot scores and cardiovascular autonomic measurements. In 24 patients, the acetylcholine sweat-spot test was abnormal, borderline in 8 and normal in three patients. Patients with hypoxaemia and peripheral sympathetic autonomic neuropathy, in conclusion. The acetylcholine sweat-spot test is repeatable, simple to carry out, and it is a good indicator of autonomic dysfunction in breathless people with COPD.

Source link: https://doi.org/10.1183/09031936.94.07061090


The thermodynamic profile and molecular interactions of a C(9)-cytisine derivative-binding acetylcholine-binding protein from Aplysia californica

The enthalpic contribution, which dominates unfavorable entropic component, drove Ac ACh's favorable titration calorimetry, according to the results. Despite the fact that ligand 4 had a less entropic effect than cytisine, Ac AChBP's affinity for Ac AChBP was significantly reduced owing to the severity of the decrease in the enthalpic component. The Ac AChBP/u2013 4 complex's high-resolution crystal structure demonstrated close similarities in the protein-u2013ligagorilla interactions involving the portions of 4 common to cytisine, suggesting close similarities in the protein-u2013ligand interactions.

Source link: https://doi.org/10.1107/s2053230x20001168


Acetylcholine activates intracellular movement of insulin granules in pancreatic beta-cells via inositol trisphosphate-dependent [correction of triphosphate-dependent] mobilization of intracellular Ca2+.

Intracellular movement of shadowy granules is a precursor to the emergence of cell-free product. Using an insulinoma cell line, MIN 6, in which acetylcholine raises both insulin secretion and granule movement, we investigated the mechanism responsible for this movement. High K+ membrane depolarization of granule movement was not reflected by Acetylcholine stimulation of granule movement. Added to acetylcholine and decreased by the Ca2+ chelator BAPTA, the phosphate formation of the endogenous myosin light chain in MIN6 cells was enhanced. These results led to the discovery that inositol trisphosphate [corrected] stimulates Ca2+ mobilization by muscarinic oxidation of PLC, resulting in intracellular transport of insulin granules to the ready-releasable pool of pancreatic beta-cells via Ca2+/calmodulin-dependent phosphorylation of myosin light chains.

Source link: https://doi.org/10.2337/diabetes.47.11.1699


Glucose and Acetylcholine Have Different Effects on the Plateau Pacemaker of Pancreatic Islet Cells

In perifused, isolated mouse islets of Langerhans, Pancreatic islet cell membrane electrical conduct has been investigated by intracellular microelectrodes. The dosereponse effects of glucose and acetylcholine on the pattern of electrical activity are compared and are shown to be qualitatively different. Periodical shifts between a polarized silence phase potential and a depolarized plateau phase with superimposed rapid spiking power are indicative of electrical activity in the presence of glucose. Moreover, rise in plateau frequency and silligence-driven spiking had no effect on the potential levels during the plateau and silent phases, while adding acetylcholine depolarized the silent phase until, with increased plateau frequency and decreased phase depolarization resulting in continuous spiking. The effects of acetylcholine and glucose are attributed to different variations on the plateau pacemaker system that controls insulin regulating.

Source link: https://doi.org/10.2337/diab.30.7.558


Restitution of Defective Glucose-Stimulated Insulin Secretion in Diabetic GK Rat by Acetylcholine Uncovers Paradoxical Stimulatory Effect of β-Cell Muscarinic Receptor Activation on cAMP Production

We have investigated AChu2019's effect on the islets of the Goto-Kakizaki rat, a spontaneous model of type 2 diabetes, because acetylcholine is a recognized source of glucose-stimulated insulin release in the normal u03b2-cell. We first established that ACh was able to restore the GK u03b2-cell's insulin secretory glucose metabolism. ACh's main function is to potently raise Ca2+-stimulated insulin production in the GK's u03b2-cell, which, in doing so, normalizes its poor glucose responsiveness.

Source link: https://doi.org/10.2337/diabetes.54.11.3229


Increased Expression of Gi-Coupled Muscarinic Acetylcholine Receptor and Gi in Atrium of Elderly Diabetic Subjects

In an ongoing research into the effects of age on human atrial tissue receptor signaling, the number of atrial muscarinic acetylcholine receptor receptors has risen with age, but not in diabetic patients, but not in diabetic patients. Since increased signaling through Gi has been shown to contribute to the development of dilated cardiomyopathy in diabetic patients with diabetes, these results point to a molecular explanation for the elevated risk of heart disease in diabetic patients.

Source link: https://doi.org/10.2337/diabetes.53.9.2392


Muscarinic Stimulation of Pancreatic Insulin and Glucagon Release Is Abolished in M3 Muscarinic Acetylcholine Receptor–Deficient Mice

Pancreatic muscarinic acetylcholine receptors play a significant role in stimulating insulin and glucagon secretion from islet cells. We first investigated the effect of insulin secretion from isolated pancreatic islets prepared from wild-type and M3 receptor-deficient mice in order to investigate the potential role of the M3 muscarinic receptor subtype in cholinergic stimulation of insulin release. Oxo-M is a stimulatory glucose level, and it greatly enhanced insulin release from islets of WT mice. M3U2212/u2212 mice had reduced serum insulin and plasma glucagon levels, as well as a significantly reduced rise in serum insulin after an oral glucose load, according to consistent with in vitro results. Despite the apparent decrease in serum glucagon levels and the fact that M3u2212/u2212 mice are hypophagic and lean, M3u2212 mice had significantly reduced blood glucose levels and even improved glucose tolerance, likely due to the reduction in plasma glucagon levels and the fact that M3u2212 mice are hypophagic and lean.

Source link: https://doi.org/10.2337/diabetes.53.7.1714


Altered Acetylcholine and Norepinephrine Concentrations in Diabetic Rat Hearts: Role of Parasympathetic Nervous System in Diabetic Cardiomyopathy

In the hearts of rats 2, 4, and 8 wk after the introduction of diabetes by a streptozocin injection, the amounts of acetylcholine as a symptom and norepinephrine as a sympathetic marker were investigated. In the diabetic rats at 2 and 4 wk, Myocardial ACh and NE concentrations were not significantly different from those in age-matched control rats. However, ACh and NE concentrations in the diabetic rats at 8 wk were noticeably higher than those in control rats. Diabetic rats at 8 wk had elevated myocardial choline and choline acetyltransferase production, acetyltransferase production, and reduced acetylcholinesterase activity, as well as decreased acetyl-hydroxyltransferase activity and decreased acetylcholinesterase activity. The findings of this research confirm a previously reported rise in sympathetic activity to the heart, as well as an increase in the synthesis and a decrease in ACh's metabolism, which shows that adequate insulin therapy normalizes these changes.

Source link: https://doi.org/10.2337/diab.38.2.231

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions