Drugs online research references
J Cell Biol. 1988 May;106(5):1703-12.
A role for acetylcholine receptors in the fusion of chick myoblasts.
Entwistle A, Zalin RJ, Warner AE, Bevan S.
Department of Anatomy and Developmental Biology, University College London, United Kingdom.
The role of acetylcholine receptors in the control of chick myoblast fusion in culture has been explored. Spontaneous fusion of myoblasts was inhibited by the nicotinic acetylcholine receptor antagonists alpha-bungarotoxin, Naja naja toxin and monoclonal antibody mcAb 5.5. The muscarinic antagonists QNB and n-methyl scopolamine were without effect. Atropine had no effect below 1 microM, where it blocks muscarinic receptors; at higher concentrations, when it blocks nicotinic receptors also, atropine inhibited myoblast fusion. The inhibitions imposed by acetylcholine receptor antagonists lasted for approximately 12 h; fusion stimulated by other endogenous substances then took over. The inhibition was limited to myoblast fusion. The increases in cell number, DNA content, the level of creatine phosphokinase activity (both total and muscle-specific isozyme) and the appearance of heavy chain myosin, which accompany muscle differentiation, followed a normal time course. Pre-fusion myoblasts, fusing myoblasts, and young myotubes specifically bound labeled alpha-bungarotoxin, indicating the presence of acetylcholine receptors. The nicotinic acetylcholine receptor agonist, carbachol, induced uptake of [14C]Guanidinium through the acetylcholine receptor. Myoblasts, aligned myoblasts and young myotubes expressed the synthetic enzyme Choline acetyltransferase and stained positively with antibodies against acetylcholine. The appearance of ChAT activity in myogenic cultures was prevented by treatment with BUDR; nonmyogenic cells in the cultures expressed ChAT at a level which was too low to account for the activity in myogenic cultures. We conclude that activation of the nicotinic acetylcholine receptor is part of the mechanism controlling spontaneous myoblast fusion and that myoblasts synthesize an endogenous, fusion-inducing agent that activates the nicotinic ACh receptor.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3372592&dopt=Abstract
Neurosci Lett. 1985 Mar 15;54(2-3):289-94.
Muscarinic acetylcholine receptors in chick heart: influence of heat and N-ethylmaleimide on receptor conformations and interactions with guanine nucleotide-dependent regulatory proteins.
Aronstam RS, Kirby ML, Smith MD.
Several conformations of muscarinic acetylcholine receptors in chick heart are revealed by the energetics of agonist binding. Heating cardiac membranes at 50 degrees C for 5 min decreased agonist affinity, steepened agonist binding curves and eliminated receptor sensitivity to guanine nucleotides. N-ethylmaleimide (NEM) steepened agonist binding curves and eliminated receptor sensitivity to guanine nucleotides without decreasing agonist binding affinity. NEM prevented and reversed the effect of heat on agonist affinity. Pirenzepine and N-methylscopolamine binding were unaffected by either treatment. NEM and heat stabilize muscarinic receptors in conformations unrelated to those associated with naturally occurring receptor populations.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3838808&dopt=Abstract
J Neurochem. 1984 Jul;43(1):33-41.
Muscarinic acetylcholine receptors in neuroblastoma cells: lack of effect of Veratrum alkaloids on receptor number.
Milligan G, Strange PG.
The effect of compounds that activate sodium channels on the number of muscarinic acetylcholine receptors in neuroblastoma NIE 115 cells has been investigated. The cells were used in electrically unexcitable ("control" cells) and excitable ("differentiated" cells) states. Although receptor assays using a single concentration of the radioligand [3H]scopolamine methyl chloride indicated a loss of receptors after a 6-h incubation of cells with veratrine, no true loss of receptors was seen with any of the compounds tested (veratridine, veratrine, aconitine) when full saturation analyses were performed in either control or differentiated cells. The apparent receptor loss seen with veratrine was due to a muscarinic receptor-active component of veratrine (not veratridine) occluded by the cells and released into the binding assays upon cell breakage. Veratridine and aconitine have a very low affinity for muscarinic acetylcholine receptors, and the binding of carbamoylcholine to the receptors is unaffected by tetrodotoxin, so that there is no evidence in this system for interaction between muscarinic receptors and sodium channels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6327920&dopt=Abstract
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