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Biophys J, August 1999, p. 758-774, Vol. 77, No. 2

Membrane Stretch Affects Gating Modes of a Skeletal Muscle Sodium Channel

Iustin V. Tabarean, Peter Juranka, and Catherine E. Morris

Departments of Medicine and Biology, University of Ottawa, and Department of Neurosciences, Loeb Health Research Institute, Ottawa Hospital, Ottawa, Ontario K1Y 4E9, Canada

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 1-3 min. Simultaneously, the faster current increased. The resulting fast current kinetics and voltage sensitivity were indistinguishable from the fast components 1) left after 10 Hz depolarizations, and 2) that dominated when alpha  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 alpha  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 alpha  subunit was directly or secondarily susceptible to bilayer tension.

Biophys J, August 1999, p. 758-774, Vol. 77, No. 2
© 1999 by the Biophysical Society   0006-3495/99/08/758/17  $2.00


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