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A mouse model of the slow channel myasthenic syndrome: Neuromuscular physiology and effects of ephedrine treatment.

Abstract:

In the slow channel congenital myasthenic syndrome mutations in genes encoding the muscle acetylcholine receptor give rise to prolonged ion channel activations. The resulting cation overload in the postsynaptic region leads to damage of synaptic structures, impaired neuromuscular transmission and fatigable muscle weakness. Previously we identified and characterised in detail the properties of the slow channel syndrome mutation εL221F. Here, using this mutation, we generate a transgenic mouse ...

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Publication status:
Published

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Authors


Webster, RG More by this author
Cossins, J More by this author
Lashley, D More by this author
Maxwell, S More by this author
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Journal:
Experimental neurology
Volume:
248
Pages:
286-298
Publication date:
2013-10-05
DOI:
EISSN:
1090-2430
ISSN:
0014-4886
URN:
uuid:2d4d8523-0c4e-4cfe-b741-07c3953874d3
Source identifiers:
407647
Local pid:
pubs:407647

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