Membrane stretch affects gating modes of a skeletal muscle sodium channel

被引:61
作者
Tabarean, IV
Juranka, P
Morris, CE
机构
[1] Ottawa Hosp, Loeb Hlth Res Inst, Dept Neurosci, Ottawa, ON K1Y 4E9, Canada
[2] Univ Ottawa, Dept Med, Ottawa, ON K1Y 4E9, Canada
[3] Univ Ottawa, Dept Biol, Ottawa, ON K1Y 4E9, Canada
基金
加拿大自然科学与工程研究理事会; 英国医学研究理事会;
关键词
D O I
10.1016/S0006-3495(99)76930-4
中图分类号
Q6 [生物物理学];
学科分类号
071011 ;
摘要
The alpha subunit of the human skeletal muscle Na+ channel recorded from cell-attached patches yielded, as expected for Xenopus oocytes,two current components that were stable for tens of minutes during 0.2 Hz stimulation. Within seconds of applying sustained stretch, however, the slower component began decreasing and, depending on stretch intensity, disappeared in 13 min. Simultaneously, the faster current increased; The resulting fast current kinetics and voltage sensitivity were indistinguishable from the fast components I) left after 10 Hz depolarizations, and 2) that dominated when ct subunit was co-expressed with human beta 1 subunit. Although high frequency depolarization-induced loss of: slow current was reversible, the stretch-induced slow-to-fast conversion was irreversible. The conclusion that stretch converted a single population of alpha subunits from an abnormal slow to a bona fide fast gating mode was confirmed by using gigaohm seals formed without suction, in which fast gating was originally absent. For brain Na+ channels, co-expressing G proteins with the channel alpha subunit yields slow gating. Because both stretch and beta 1 subunits induced the fast gating mode, perhaps they do so by minimizing a subunit interactions with G proteins or with other regulatory molecules available in oocyte membrane. Because of the possible involvement of oocyte molecules, it remains to be determined whether the Na+ channel a subunit was directly or secondarily susceptible to bilayer tension.
引用
收藏
页码:758 / 774
页数:17
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