Disease relevance of Bromoacetylcholine

• Immunology of acetylcholine receptors in relation to myasthenia gravis [1].
• Lambert-Eaton myasthenic syndrome is characterized by muscle weakness, hyporeflexia, and autonomic dysfunction, which result from impaired release of acetylcholine from cholinergic nerve terminals [2].
• In contrast, all eight of the arteries with advanced stenoses showed dose-dependent constriction, from 1.05 +/- 0.05 to 0.32 +/- 0.16 mm at the highest concentration of acetylcholine (P less than 0.01), with temporary occlusion in five [3].
• Our preliminary findings suggest that the abnormal vascular response to acetylcholine may represent a defect in endothelial vasodilator function, and may be important in the pathogenesis of coronary vasospasm [3].
• Generalized epilepsy with febrile seizures plus (GEFS+), benign familial neonatal convulsions and nocturnal frontal lobe epilepsy, three autosomal dominant idiopathic epilepsies, result from mutations affecting voltage-gated sodium and potassium channels, and nicotinic acetylcholine receptors, respectively [4].

Psychiatry related information on Bromoacetylcholine

• To study acetylcholine synthesis, we measured the incorporation of radiolabeled glucose into the transmitter in temporal-cortex specimens obtained at diagnostic craniotomy in 17 young patients with Alzheimer's disease [5].
• However, despite clear biochemical and anatomical evidence for a fall in ACh in dementia, results of therapeutic trials with cholinergic agonists, precursors and cholinesterase inhibitors have been inconsistent [6].
• We also show that these neurons are inhibited by noradrenaline and acetylcholine, both of which are transmitters of wakefulness [7].
• Curiously, inhibitors of the acetylcholine-hydrolysing enzyme acetylcholinesterase may induce psychopathologies that are reminiscent of PTSD [8].
• Arecholine (4 milligrams), a cholinergic agonist, and choline (10 grams), a precursor of acetylcholine, significantly enhanced serial learning in normal human subjects [9].

High impact information on Bromoacetylcholine

• These nicotinic antagonist peptides from Conus are broadly divided into two groups: those that act at the neuromuscular junction and those that act at subtypes of neuronal nicotinic acetylcholine receptors [10].
• Depending on the preparation (cultured cells, adrenal slices) and the stimulation pattern (action potentials, depolarizing pulses, high K(+), acetylcholine), the role of each calcium channel in controlling catecholamine release can change drastically [11].
• The receptors include the photopigments such as rhodopsin and prominent families such as the adrenergic, muscarinic acetylcholine, and chemokine receptors involved in regulating a broad spectrum of responses in humans [12].
• Acetylcholine receptor gene expression at the developing neuromuscular junction [13].
• Control of acetylcholine receptors in skeletal muscle [14].

Chemical compound and disease context of Bromoacetylcholine

• The disruption of the balance between the functions of GABA, dopamine, and acetylcholine neurons in the extrapyramidal system probably accounts for some of the symptoms observed in the Lesch-Nyhan syndrome (e.g., choreoathetosis) [15].
• By contrast, rings from patients with chronic obstructive lung disease achieved only 41.3 +/- 4.8 percent of maximal relaxation in response to acetylcholine (n = 32) and 49.4 +/- 5.5 percent in response to adenosine diphosphate (n = 24) (P less than 0.001, as compared with control rings) [16].
• Direct binding of the rabies virus glycoprotein to the acetylcholine receptor could contribute to the neurotropism of this virus [17].
• In vivo imaging of muscarinic acetylcholine receptor binding function in a patient with Alzheimer's disease, using single-photon emission computed tomography and iodine 123-labeled 3-quinuclidinyl-4-iodobenzilate (123I-QNB), and perfusion imaging using 123I-N-isopropyl p-iodoamphetamine are described [18].
• Responses to bradykinin were similar in vessels from normal pregnant and preeclamptic women while those to acetylcholine were absent in vessels from women with preeclampsia [19].

Biological context of Bromoacetylcholine

• The integrity of these fibers was assessed objectively by measuring axon reflex vasodilation in response to stimulation with 10 percent acetylcholine introduced by electrophoresis [20].
• The total number of alpha-bungarotoxin binding sites was reduced by 30% in the presence of carbachol, indicating that this agent affects the rate of synthesis of the acetylcholine receptor [21].
• METHODS: We randomly assigned 19 patients with coronary endothelial dysfunction, indicated by abnormal acetylcholine-induced vasoconstriction, to an exercise-training group (10 patients) or a control group (9 patients) [22].
• The kinetics of labeling of the "pool" and "surface" receptors with 2H, 13C, 15N-amino acids confirm the "precursor-product" type relationship of pool and surface acetylcholine receptors [23].
• The responses of blood flow and vascular resistance to acetylcholine were significantly reduced in the hypertensive patients (P less than 0.0001); maximal forearm flow was 9.1 +/- 5 ml per minute per 100 ml in the patients and 20.0 +/- 8 ml per minute per 100 ml in the controls (P less than 0.0002) [24].

Anatomical context of Bromoacetylcholine

• Endothelium-dependent coronary-artery vasomotion in response to an intracoronary infusion of acetylcholine (10(-8) to 10(-6) M) was assessed at base line and after one year of therapy [25].
• By contrast, if the endothelium is removed experimentally, acetylcholine constricts blood vessels [3].
• Degradation of the acetylcholine receptor in cultured muscle cells: selective inhibitors and the fate of undegraded receptors [26].
• Direct observation of the rapid aggregation of acetylcholine receptors on identified cultured myotubes after exposure to embryonic brain extract [27].
• Xenopus oocytes injected with alpha 9 cRNA express a homomeric receptor-channel complex that is activated by acetylcholine [28].

Associations of Bromoacetylcholine with other chemical compounds

• In the mammary artery, relaxation was greatest in response to acetylcholine (86 +/- 4 percent reduction in norepinephrine-induced tension), followed by thrombin (44 +/- 7 percent) and adenosine diphosphate (39 +/- 8 percent) [29].
• Choline is the physiologic precursor of acetylcholine, and its administration elevates brain acetylcholine levels in laboratory animals and, possibly, in human beings [30].
• In addition, the samples were assayed for the gamma-aminobutyric-acid-synthesizing enzyme, glutamic acid decarboxylase, and for the acetylcholine-synthesizing enzyme, choline acetyltransferase [31].
• Furthermore, in 293 cells expressing Kv1.2 and ml muscarinic acetylcholine receptors, inactivating RhoA using C3 exoenzyme blocked the ability of ml receptors to suppress Kv1.2 current [32].
• DMSO (2%) inhibits the fusion of myoblasts to form multinucleate myotubes, the normal increases in activity of creatine phosphokinase (CPK) and acetylcholinesterase, and the synthesis of alpha-actin and acetylcholine receptor protein [33].

Gene context of Bromoacetylcholine

• The neuronal nicotinic acetylcholine receptor alpha 4 subunit (CHRNA4) maps to the same region of 20q (ref. 12) and the gene is expressed in all layers of the frontal cortex [34].
• Mice lacking the M3 muscarinic acetylcholine receptor are hypophagic and lean [35].
• The Caenorhabditis elegans unc-17 gene: a putative vesicular acetylcholine transporter [36].
• STAT3 was phosphorylated by the tyrosine kinase Jak2 that was recruited to the alpha7 subunit of the nicotinic acetylcholine receptor [37].
• Administration of anti-IL-4 only during the period of the aerosol challenge did not affect the subsequent response to acetylcholine [38].

Analytical, diagnostic and therapeutic context of Bromoacetylcholine

• There were no significant differences between the two groups with respect to hemodynamic variables at rest and during exercise, risk factors for ischemic heart disease, findings on magnetic resonance imaging and radionuclide perfusion studies of the heart, or changes in brachial flow during the infusion of acetylcholine [39].
• The degree of constriction or dilation during mental stress correlated with the response to the infusions of acetylcholine (P less than 0.0003, r = 0.58) [40].
• After four weeks of exercise, the increases in response to acetylcholine were 27+/-7, 73+/-19, and 142+/-28 percent (P<0.01 for the comparison with the control group) [22].
• At the initial and follow-up studies, patients received serial intracoronary infusions (in a coronary artery not undergoing angioplasty) of acetylcholine to assess endothelium-mediated vasodilatation [41].
• We have studied assembly of acetylcholine receptor in vivo using subunit-specific monoclonal antibodies and immunoprecipitation with alpha-bungarotoxin and antitoxin [42].

References