Muscle acetylcholine receptor

Tsouloufis et al.8 used an ELISA to assess the refolding of a recombinant subunit of the extracellular domain of the human muscle acetylcholine receptor expressed in E. coli. The plates were coated with refolded or unfolded protein and then reacted with conformationally dependent MAbs. The use of specific... 

Tsouloufis, T., A. Mamalaki, M. Remoundos, and S.J. Tzartos (2000). Reconstitution of conformationally dependent epitopes on the N-terminal extracellular domain of the human muscle acetylcholine receptor alpha subunit expressed in Escherichia colt implications for myasthenia gravis therapeutic approaches. Int Immunol 12(9) 1255-1265. 

Niu L, Abood LG, Hess GP (1995) Cocaine mechanism of inhibition of a muscle acetylcholine receptor studied by a laser-pulse photolysis technique. Proc Natl Acad Sci USA 92 12008-12012... 

Mishina, M., Takai, T., Imito, K., Noda, M., Takahashi, T., Numa, S., Methfessel, C., Sakmann, B. (1986). Molecular distinction between fetal and adult forms of muscle acetylcholine receptor. Nature 321 406-11. 

In myasthenia gravis synaptic transmission at the neuromuscular junction is impaired most cases have an autoimmune basis and some 85% of patients have a raised titre of autoantibodies to the muscle acetylcholine receptor. The condition is probably heterogeneous, however, as about 15% do not have receptor antibodies, or have antibodies to another neuromuscular junction protein (muscle specific kinase) and rarely it occurs with penicillamine used for rheumatoid arthritis. 

Martyn JA, White DA, Gronert GA, Jaffe RS, Ward JM. Up-and-down regnlation of skeletal muscle acetylcholine receptors. Effects on nenromuscular blockers. Anesthesiology 1992 76(5) 822-43. 

Koltgen D, Ceballos-Baumann AO, Franke C. Botuhnum toxin converts muscle acetylcholine receptors from adult to embryonic type. Muscle Nerve 1994 17(7) 779-84. 

D. Succinylcholine may produce hyperkalemia in patients with neuropathy, myopathy, recent severe bums, or head and spin cord injury (this risk is maximal a few months after the injury). The mechanism is increased extr unc-tional muscle acetylcholine receptors and may also occur with prolonged use of nondepolarizing agents. 

Evans, S. D., Goldman, S., Heinemann, S., and Patrick, J., 1987, Muscle acetylcholine receptor biosynthesis, J. Biol. Chem. 262 4911-4916. 

Merlie, R, and Lindstorm, J., 1983, Assembly in vivo of mouse muscle acetylcholine receptor Identification of an a-subunit species that may be an assembly intermediate, Cell 34 747-757. 

New, H. V., and Mudge, A. W., 1986, Calcitonin gene-related peptide regulates muscle acetylcholine receptor synthesis. Nature 323 809-811. 

Autoantibodies are directed against nicotinic acetylcholine receptors in myasthenia gravis, resulting in receptor loss, skeletal muscle paralysis, and dysfunction (100). In addition, antibodies directed against voltage-gated Ca " channels produce similar neuromuscular dysfunction of Lambert-Eaton... 

Paton, W. D. M., and Rang, H. P. (1965). The uptake of atropine and related drags by intestinal smooth muscle of the guinea pig in relation to acetylcholine receptors. Proc. R. Soc. Lond. [Biot.] 163 1-44. 

Nicotinic receptors (nicotinic acetylcholine receptors, nACHR) exist not only in the membrane of vertebrate skeletal muscle at the synapse between nerve and muscle (muscle-type nAChR) but also at various synapses throughout the brain, mainly at presynaptic positions (neuronal-type nAChR). Whereas the muscle-type nAChR is precisely composed of two a 1-subunits, one (3 -subunit, one y -subunit and one y -subunit (adult)... 

D-penicillamine a well-recognized complication of the use of D-penicillamine is a myasthenic syndrome. Most reported cases of myasthenic syndrome are women and the ocular muscles appear to be particularly commonly affected at early stages of the abnormality. The onset of the myasthenic syndrome can range between a few months and many years, and is not always reversible. There is a clear immunological basis to this problem, because it is associated with raised anti-acetylcholine receptor antibodies circulating in the serum. Antibody levels fall when the drug is withdrawn, and this, in turn, is associated with clinical improvement. How the... 

These include nicotinic acetylcholine receptors, neuronal calcium channels, muscle sodium channels, vasopressin receptors, and iV-methyl-D-aspartate (NMDA) receptors. Some general features of the structure, function, and evolution of biologically active peptides isolated from Conus venom are presented. 

In the venom of C. geographus and other fish-hunting species, the conotoxins isolated so far can be divided into three major classes (1-4) o -conotoxms which block neuronal calcium channels at the presynaptic terminus of the neuromuscular junction, a-conotoxins which inhibit the acetylcholine receptor at the postsynaptic terminus, and x-conotoxins which block Na channels on the muscle membrane. 

Peptides in the a-conotoxin family are inhibitors of nicotinic acetylcholine receptors. They were first isolated from C. geographus venom as components which cause paralysis in mice and fish when injected intraperitoneally (27). Early physiological experiments (28) indicated that a-conotoxins GI, GII, and GIA (see Table III) all act at the muscle end plate region. Mini end-plate potentials and end plate potentials evoked in response to nerve stimulation are inhibited in the presence of a-conotoxins in the nM to pM range. a-Conotoxin GI was subsequently shown to compete with rf-tubocurarine and a-bungarotoxin for the acetylcholine receptor (29). 

When a nerve-muscle preparation is stimulated in the presence of a sea snake neurotoxin, there is no twitch. However, when the muscle itself is stimulated directly in the presence of a neurotoxin, the muscle contracts. This means that neurotoxin does not inhibit the muscle itself. Moreover, postsynaptic neurotoxin does not inhibit the release of acetylcholine from the nerve ending. Therefore, the site of snake toxin inhibition must be in the postsynaptic site 20). Later it was shown that a neurotoxin strongly binds to the acetylcholine receptor (AChR). 

Edmonds, B., Gibb, A. J., and Colquhoun, D., Mechanisms of activation of muscle nicotinic acetylcholine receptors and the time course of endplate currents, Annu. Rev. Physiol., 57, 469-493, 1995. 

Lingle, C. L., Maconochie, D., and Steinbach, J. H., Activation of skeletal muscle nicotinic acetylcholine receptors, J. Memb. Biol., 126, 195-217, 1992 (excellent review of much of the evidence concerning the mechanism of receptor activation). 

Lindstrom, J.M. Nicotinic acetylcholine receptors of muscles and nerves comparison of their structures, functional roles, and vulnerability to pathology. Ann. N.Y. Acad. Sci. 998 41, 2003. 

It has been known for some time that the enteric nervous system does not simply regulate smooth muscle contraction, but is intimately involved in the control of transport processes in enterocytes. Nerve fibres in the mucosa terminate subjacent to the basement membrane of epithelial and entero-endocrine cells, on which muscarinic acetylcholine receptors (mAChRs)... 

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