Calcium current activation and charge movement in denervated mammalian skeletal muscle fibres.

Delbono, Osvaldo

doi:10.1113/jphysiol.1992.sp019160

Cited by 61 publications

(85 citation statements)

References 41 publications

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“…Whether excitation-contraction uncoupling results from alterations in neural control of muscle gene expression is not known at the present time. However, a series of studies have supported this concept: for example, denervation results in a significant decrease in DHPR functional expression and alterations in excitation-contraction coupling in skeletal muscle from adult rats (Delbono, 1992); nerve crush leads to reduction in the levels of mRNA encoding DHPR subunits and RyR1 in muscle (Ray et al ., 1995); also, there are indications that both DHPR and RyR1 expression are dependent on skeletal muscle innervation (Kyselovic et al ., 1994;Pereon et al ., 1997b); during development, DHPR mRNA levels change in relation with fibre innervation (Chaudari & Beam, 1993); myotube depolarization triggers the appearance of (+)-[ 3 H]PN 200 -110 binding sites (Pauwels et al ., 1987); and, finally, exercise and chronic stimulation in vivo increase the expression of DHPR in homogenates of soleus and EDL muscles (Saborido et al ., 1995;Pereon et al ., 1997a). These studies support the concept that fibre-type composition, DHPR and RyR1, and excitationcontraction coupling depend on nerve stimulation and muscle activity.…”

Section: Excitation-contraction Uncouplingmentioning

confidence: 99%

“…Several groups have reported skeletal muscle denervation and re-innervation, motor unit remodelling or loss in aging rodents or humans (Hashizume et al ., 1988;Kanda & Hashizume, 1989, 1992Einsiedel & Luff, 1992;Doherty et al ., 1993;Johnson et al ., 1995;Zhang et al ., 1996). Motor unit remodelling leads to changes in fibre-type composition (Pette & Staron, 2001).…”

Section: Neural Influences On Aging Skeletal Musclementioning

confidence: 99%

“…Experimental denervation of skeletal muscle leads to a series of changes in skeletal muscles from aging rodents, such as reorientation of costameres (rib-like structures formed by dystrophin and β -dystroglycan) (Bezakova & Lomo, 2001), proliferation of triadic membranes (Salvatori et al ., 1988), decrease in charge movement (functional expression of the dihydropyridine receptor voltage sensor) and alterations in the sarcoplasmic reticulum calcium release channel (Delbono, 1992;Delbono & Stefani, 1993;Delbono & Chu, 1995;Delbono et al ., 1997;Wang et al ., 2000). We hypothesize that age-related denervation (see above) may induce these structural and functional changes in mammalian muscle, including in humans.…”

Section: Plasticity At the Neuromuscular Junctionmentioning

confidence: 99%

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Neural control of aging skeletal muscle

2003

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SummaryFunctional and structural decline in the neuromuscular system with aging has been recognized as a cause of impairment in physical performance and loss of independence in the elderly. Alterations in spinal cord motor neurones and at the neuromuscular junction have been identified as evidence of denervation in skeletal muscles from aging mammals, including humans. However, the reciprocal influences of neurones on gene expression in muscle and of muscle on age-related neurodegeneration are poorly understood, and, as a result, interventions aimed at delaying or preventing degeneration of the neural component in aging muscle have been largely unsuccessful. The present article discusses the evidence for neural influence on age-related impairments of skeletal muscle, including a role in excitation-contraction uncoupling. The role of nerves in regulating the trophic actions of insulin-like growth factor-1 (IGF-1) and other neurotrophic factors is considered as a novel influence on the effects of aging on the neuromuscular junction. A better understanding of nerve-muscle interactions will allow for more rational interventions in the aging neuromuscular system.

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Section: Excitation-contraction Uncouplingmentioning

confidence: 99%

Section: Neural Influences On Aging Skeletal Musclementioning

confidence: 99%

Section: Plasticity At the Neuromuscular Junctionmentioning

confidence: 99%

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Neural control of aging skeletal muscle

2003

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“…In addition they permit an extremely slow calcium inward current (L_type current) whose physiological role is still unclear (for a review see Melzer et al 1995). L_type current characteristics have been extensively studied in adult amphibian and mammalian skeletal muscle (for references see Delbono, 1992;Feldmeyer et al 1990Feldmeyer et al , 1992Feldmeyer et al , 1995Garcia et al 1992;Francini et al 1996). On the other hand, important data on structure-function relationships of the channel have been obtained by heterologous expression of recombinant DHP receptors in cultured immature muscle cells (myotubes) (Tanabe et al 1988;Garcia et al 1994).…”

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confidence: 99%

Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Harasztosi

Sipos

Kovács

et al. 1999

The Journal of Physiology

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1. Inactivation and recovery kinetics of L_type calcium currents were measured in myotubes derived from satellite cells of human skeletal muscle using the whole cell patch clamp technique. 2. The time course of inactivation at potentials above the activation threshold was obtained from the decay of the current during 15 s depolarizing pulses. At subthreshold potentials, prepulses of different durations, followed by +20 mV test pulses, were used. The time course could be well described by single exponential functions of time. The time constant decreased from 17·8 ± 7·5 s at −30 mV to 1·78 ± 0·15 s at +50 mV. 3. Restoration from inactivation caused by 15 s depolarization to +20 mV was slowed by depolarization in the restoration interval. The time constant increased from 1·11 ± 0·17 s at −90 mV to 7·57 ± 2·54 s at −10 mV. 4. Restoration showed different kinetics depending on the duration of the conditioning depolarization. While the time constant was similar at restoration potentials of −90 and −50 mV after a 1 s conditioning prepulse, it increased with increasing prepulse duration at −50 mV and decreased at −90 mV. 5. The experiments showed that the rates of inactivation and restoration of the L_type calcium current in human myotubes were not identical when observed at the same potential. The results indicate the presence of more than one inactivated state and point to different voltage-dependent pathways for inactivation and restoration.8422

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“…The progress of muscle atrophy in denervated muscle is time dependent. In mammals changes of the passive electrical properties of the sarcolemma [15], in transverse tubules organization [68], sarcolemmal Ca 2+ current, and the ability to sustain tension during prolonged contractions [19] were just observed in the first weeks after muscle denervation. Muscle atrophy advances faster in the early weeks after denervation but then progresses slower and it may reach a steady-state that is maintained for long time [2,62].…”

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confidence: 99%

Excitation-contraction coupling and mechano-sensitivity in denervated skeletal muscles

Francini

Squecco

2010

Eur J Transl Myol

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Skeletal muscle atrophy can be defined as a wasting or decrease in muscle mass and muscle force generation owing lack of use, ageing, injury or disease. Thus, the etiology of atrophy can be different. Atrophy in denervated muscle is a consequence of two factors: 1) the complete lack of motoneuron activity inducing the deficiency of neurotransmitter release and 2) the muscles disuse. The balance of the muscular functions depends on extra-and intra-muscular signals. In the balance are involved the excitation-contraction coupling (ECC), local growth factors, Ca 2+ -dependent and independent intracellular signals, mechano-sensitivity and mechano-transduction that activate Ca 2+ -dependent signaling proteins and cytoskeletonnucleus pathways to the nucleus, that regulate the gene expression. Moreover, retrograde signal from intracellular compartments and cytoskeleton to the sarcolemma are additional factors that regulate the muscle function. Proteolytic systems that operate in atrophic muscles progressively reduce the muscle protein content and so the sarcolemma, ECC and the force generation. In this review we will focus on the more relevant changes of the sarcolemma, excitation-contraction coupling, ECC and mechano-transduction evaluated by electrophysiological methods and observed from early-to long-term denervated skeletal muscles. This review put in particular evidence that long-term denervated muscle maintain a sub-population of fibers with ECC and contractile machinery able to be activated, albeit in lesser amounts, by electrical and mechanical stimulation. Accordingly, this provides a potential molecular explanation of the muscle recovery that occurs in response to rehabilitation strategy as transcutaneous electrical stimulation and passive stretching of denervated muscles, which wre developed as a result of empirical clinical observations. Key Words: Excitation-contraction coupling; L-type Ca 2+ current; Mechano-transduction; Skeletal muscle; Long-term denervation European Journal Translational Myology -Myology Reviews 2010; 1 (3): 121-130 Skeletal muscle atrophy can be defined as a wasting or decrease in muscle mass and muscle force generation owing lack of use, ageing, injury, or disease. Thus, the etiology of atrophy can be different. Atrophy resulting from disuse (muscle unloading, immobilization, bed rest, and spaceflight) and described as acute atrophy, is readily reversible by exercise and is the consequence of the lack of muscle activity that reduced the gene activation and protein synthesis. The age-related loss of muscle mass and strength, sarcopenia, may be considered to be chronic. Muscle atrophy resulting from chronic disease rather than disuse is described as cachexia and generally arises either from permanent damage of motoneurons or from muscle diseases. Both causes can be the result of either genetic abnormality of nerves or muscles, or systemic diseases. In motoneuron pathology muscle Excitation-contraction coupling in denervated muscleEuropean Journal Translational Myology -Myolo...

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Calcium current activation and charge movement in denervated mammalian skeletal muscle fibres.

Cited by 61 publications

References 41 publications

Neural control of aging skeletal muscle

Neural control of aging skeletal muscle

Kinetics of inactivation and restoration from inactivation of the L‐type calcium current in human myotubes

Excitation-contraction coupling and mechano-sensitivity in denervated skeletal muscles

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