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Effects of temperature on slow and fast inactivation of rat skeletal muscle Na+ channels
Departments of Neurology and Neuroscience, Case Western Reserve University School of Medicine, Louis Stokes Cleveland Veterans Affairs Medical Center, University Hospitals of Cleveland, Cleveland, Ohio 44106 Patch-clamp studies of mammalian skeletal muscle Na + channels are commonly done at subphysi...
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Published in: | American Journal of Physiology: Cell Physiology 1999-11, Vol.277 (5), p.C937-C947 |
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Main Author: | |
Format: | Article |
Language: | English |
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Online Access: | Get full text |
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Summary: | Departments of Neurology and Neuroscience, Case Western Reserve
University School of Medicine, Louis Stokes Cleveland Veterans
Affairs Medical Center, University Hospitals of Cleveland,
Cleveland, Ohio 44106
Patch-clamp
studies of mammalian skeletal muscle
Na + channels are commonly done at
subphysiological temperatures, usually room temperature. However, at
subphysiological temperatures, most
Na + channels are inactivated at
the cell resting potential. This study examined the effects of
temperature on fast and slow inactivation of
Na + channels to determine if
temperature changed the fraction of Na + channels that were excitable
at resting potential. The loose patch voltage clamp recorded
Na + currents
( I Na ) in vitro
at 19, 25, 31, and 37°C from the sarcolemma of rat type IIb
fast-twitch omohyoid skeletal muscle fibers. Temperature affected the
fraction of Na + channels that were
excitable at the resting potential. At 19°C, only 30% of channels
were excitable at the resting potential. In contrast, at 37°C, 93%
of Na + channels were excitable at
the resting potential. Temperature did not alter the resting potential
or the voltage dependencies of activation or fast inactivation.
I Na available at
the resting potential increased with temperature because the
steady-state voltage dependence of slow inactivation shifted in a
depolarizing direction with increasing temperature. The membrane
potential at which half of the Na +
channels were in the slow inactivated state was shifted by +16 mV at
37°C compared with 19°C. Consequently, the low availability of
excitable Na + channels at
subphysiological temperatures resulted from channels being in the slow,
inactivated state at the resting potential.
mammalian skeletal muscle; sodium channel; sodium current; fast
inactivation; slow inactivation; paramyotonia congenita; hyperkalemic
periodic paralysis |
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ISSN: | 0363-6143 1522-1563 |
DOI: | 10.1152/ajpcell.1999.277.5.c937 |