Abstract：
:Two mutations in the sodium channel alpha subunit that have been implicated as the cause of periodic paralysis were studied by functional expression in a mammalian cell line. Both mutations disrupted inactivation without affecting the time course of the onset of the sodium current or the single-channel conductance. This is the same functional defect that was observed in myotubes cultured from affected patients and proves that these mutations are not benign polymorphisms. Unlike the currents in the myotubes, however, there was no consistent potassium dependence for the noninactivating component. These mutations also define new regions of the sodium channel alpha subunit that are involved in the process of inactivation.
journal_name
Neuronjournal_title
Neuronauthors
Cannon SC,Strittmatter SMdoi
10.1016/0896-6273(93)90321-hsubject
Has Abstractpub_date
1993-02-01 00:00:00pages
317-26issue
2eissn
0896-6273issn
1097-4199pii
0896-6273(93)90321-Hjournal_volume
10pub_type
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