Abstract：
:Normokalemic periodic paralysis (normoPP) is a type of skeletal muscle function disorder which is characterized by paralysis attack with concomitant normal serum potassium level. We previously reported that R675Q mutation of human skeletal muscle voltage-gated sodium channel α subunit (SCN4A) may be the novel mutation which caused normoPP in Chinese families. However, it is still not clear how this mutation affects the SCN4A channel function. In this study, we used patch-clamp recording to study the function of wild type (WT) and R675Q mutant of SCN4A channels expressed in human embryonic kidney (HEK293) cells. We found that R675Q mutation did not affect the voltage dependence of sodium channel activation. The fast inactivation was also not significantly affected by R675Q mutation. However, R675Q mutation of SCN4A channels exhibited an 11.1 mV hyperpolarized shift in the voltage dependence of slow inactivation and significantly prolonged the recovery from prolonged inactivation state. Our results thus indicate that SCN4A was functionally affected by R675Q mutation, suggesting a possible reason for causing normoPP in Chinese patients.
journal_name
Cell Mol Neurobioljournal_title
Cellular and molecular neurobiologyauthors
Wu L,Zhang B,Kang Y,Wu Wdoi
10.1007/s10571-014-0052-ysubject
Has Abstractpub_date
2014-07-01 00:00:00pages
707-14issue
5eissn
0272-4340issn
1573-6830journal_volume
34pub_type
杂志文章abstract：:Depression is a major psychiatric disorder affecting nearly 21% of the world population and imposes a substantial health burden on society. Although significant progress has been made in depression research, the common molecular mechanism of antidepressants is still far from clearly understood. The neuroprotective eff...
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journal_title：Cellular and molecular neurobiology
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