Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

Sherman, Scott J.; Catterall, William A.

doi:10.1073/pnas.81.1.262

Cited by 86 publications

(47 citation statements)

References 32 publications

(47 reference statements)

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“…This finding is in disagreement with the results of numerous other studies (34,50) in which the investigators found a decrease in Na ϩ current densities caused by ionophore treatment. In our study, with the use of comparably low ionophore concentrations, upregulation of Na v 1.5 seems to compensate for downregulation of Na v 1.4, which may result in similar Na ϩ current densities.…”

Section: A-23187 Treatment Causes Fast-to-slow Fiber Type Conversioncontrasting

confidence: 57%

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C₂C₁₂ skeletal muscle cells

Zebedin

Sandtner²,

Galler³

et al. 2004

American Journal of Physiology-Cell Physiology

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. Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C2C12 skeletal muscle cells. Am J Physiol Cell Physiol 287: C270 -C280, 2004. First published March 24, 2004 10.1152/ ajpcell.00015.2004.-Each skeletal muscle of the body contains a unique composition of "fast" and "slow" muscle fibers, each of which is specialized for certain challenges. This composition is not static, and the muscle fibers are capable of adapting their molecular composition by altered gene expression (i.e., fiber type conversion). Whereas changes in the expression of contractile proteins and metabolic enzymes in the course of fiber type conversion are well described, little is known about possible adaptations in the electrophysiological properties of skeletal muscle cells. Such adaptations may involve changes in the expression and/or function of ion channels. In this study, we investigated the effects of fast-to-slow fiber type conversion on currents via voltage-gated Na ϩ channels in the C2C12 murine skeletal muscle cell line. Prolonged treatment of cells with 25 nM of the Ca 2ϩ ionophore A-23187 caused a significant shift in myosin heavy chain isoform expression from the fast toward the slow isoform, indicating fast-to-slow fiber type conversion. Moreover, Na ϩ current inactivation was significantly altered. Slow inactivation less strongly inhibited the Na ϩ currents of fast-to-slow fiber type-converted cells. Compared with control cells, the Na ϩ currents of converted cells were more resistant to block by tetrodotoxin, suggesting enhanced relative expression of the cardiac Na ϩ channel isoform Nav1.5 compared with the skeletal muscle isoform Na v1.4. These results imply that fast-toslow fiber type conversion of skeletal muscle cells involves functional adaptation of their electrophysiological properties. muscle plasticity; myosin heavy chain expression; sodium channel expression ADULT SKELETAL MUSCLE has a remarkable capacity to adapt in response to altered functional demands such as enhanced activity or disuse. On the basis of contraction kinetics, a distinction is drawn between "fast" and "slow" skeletal muscles, which contain predominantly fast-and slow-type muscle fibers, respectively. These fiber types express specific sets of fast and slow protein isoforms (for review, see Refs. 5,36,47) and are generally categorized according to the specific myosin heavy chain (MHC) isoforms that they express. In adaptation to altered functional demands, muscle fibers can switch from the fast to the slow fiber type and vice versa (i.e., fiber type conversion). Fiber type conversion involves morphological and biochemical changes that result in altered contractile properties and endurance capacities. It is well established that motor neuron firing patterns control the expression of isoforms of contractile proteins and metabolic enzymes of muscle fibers in vivo (6, 44). These firing patterns have been mimicked successfully in vitro in cell culture studies by imposed electrical stimulation (28, 58). The cellular s...

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Section: A-23187 Treatment Causes Fast-to-slow Fiber Type Conversioncontrasting

confidence: 57%

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C₂C₁₂ skeletal muscle cells

Zebedin

Sandtner²,

Galler³

et al. 2004

American Journal of Physiology-Cell Physiology

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“…Na ϩ currents in developing cortical neurons also show a corresponding upregulation when electrical activity is blocked chronically with TTX (143). Similar activity-dependent downregulation of Na ϩ channels occurs in skeletal and cardiac muscle cells (77,105,452,538), where there is direct evidence that the effects are secondary to Ca 2ϩ entry. Activity has been reported to upregulate Na ϩ channel density in a Ca 2ϩ -dependent manner in GH3 cells (417 (528).…”

Section: ؉ -Gated Channelsmentioning

confidence: 86%

Ion Channel Development, Spontaneous Activity, and Activity-Dependent Development in Nerve and Muscle Cells

Moody¹,

Bosma²

2005

Physiological Reviews

341

323

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At specific stages of development, nerve and muscle cells generate spontaneous electrical activity that is required for normal maturation of intrinsic excitability and synaptic connectivity. The patterns of this spontaneous activity are not simply immature versions of the mature activity, but rather are highly specialized to initiate and control many aspects of neuronal development. The configuration of voltage- and ligand-gated ion channels that are expressed early in development regulate the timing and waveform of this activity. They also regulate Ca2+ influx during spontaneous activity, which is the first step in triggering activity-dependent developmental programs. For these reasons, the properties of voltage- and ligand-gated ion channels expressed by developing neurons and muscle cells often differ markedly from those of adult cells. When viewed from this perspective, the reasons for complex patterns of ion channel emergence and regression during development become much clearer.

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“…The fact that Na+ channels must be functional to have this effect suggests that the expression of muscle K+ channels may be sensitive to electrical activity, as is the case, for example, for the mammalian skeletal muscle Na+ channel (Sherman & Catterall, 1984). The increase in K+ channel expression seen would tend to compensate for the excitatory effects of early Na+ channel expression.…”

Section: Discussionmentioning

confidence: 99%

Na+ channel mis‐expression accelerates K+ channel development in embryonic Xenopus laevis skeletal muscle.

Linsdell

Moody

1994

The Journal of Physiology

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1. The normal developmental pattern of voltage‐gated ion channel expression in embryonic skeletal muscle cells of the frog Xenopus laevis was disrupted by introduction of cloned rat brain Na+ channels. 2. Following injection of channel mRNA into fertilized eggs, large Na+ currents were observed in muscle cells at the earliest developmental stage at which they could be uniquely identified. Muscle cells normally have no voltage‐gated currents at this stage. 3. Muscle cells expressing exogenous Na+ channels showed increased expression of at least two classes of endogenous K+ currents. 4. This increase in K+ current expression was inhibited by the Na+ channel blocker tetrodotoxin, suggesting that increased electrical activity caused by Na+ channel mis‐expression triggers a compensatory increase in K+ channel expression. 5. Block of endogenous Na+ channels in later control myocytes retards K+ current development, indicating that a similar compensatory mechanism to that triggered by Na+ channel mis‐expression operates to balance Na+ and K+ current densities during normal muscle development.

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Electrical activity and cytosolic calcium regulate levels of tetrodotoxin-sensitive sodium channels in cultured rat muscle cells.

Cited by 86 publications

References 32 publications

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C₂C₁₂ skeletal muscle cells

Fiber type conversion alters inactivation of voltage-dependent sodium currents in murine C₂C₁₂ skeletal muscle cells

Ion Channel Development, Spontaneous Activity, and Activity-Dependent Development in Nerve and Muscle Cells

Na+ channel mis‐expression accelerates K+ channel development in embryonic Xenopus laevis skeletal muscle.

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