ArticleBiophysical journal2000
L-Type Ca(2+) channel charge movement and intracellular Ca(2+) in skeletal muscle fibers from aging mice.
Article in Biophysical journal, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.
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Who cites it
52 citing papers in PubMed.
- Aging induces sarcopenia by disrupting the crosstalk between the skeletal muscle microenvironment and myofibers.Journal of advanced research · 2026Review
- Molecular Framework of the Onset and Progression of Skeletal Muscle Aging.International journal of molecular sciences · 2025Review
- Effects of aging on calcium channels in skeletal muscle.Frontiers in molecular biosciences · 2025Review
- Sarcoplasmic Reticulum CaCells · 2023Review
- Understanding altered contractile properties in advanced age: insights from a systematic muscle modelling approach.Biomechanics and modeling in mechanobiology · 2023Article
- Voltage-dependent CaAmerican journal of physiology. Cell physiology · 2022Article
- The emerging role of the sympathetic nervous system in skeletal muscle motor innervation and sarcopenia.Ageing research reviews · 2021Review
- Equivalent L-type channel (CaBiochemical and biophysical research communications · 2020Article
- Skeletal Muscle Hypertrophy, Insulin-like Growth Factor 1, Myostatin and Follistatin in Healthy and Sarcopenic Elderly Men: The Effect of Whole-body Resistance Training.International journal of preventive medicine · 2019Article
- Aging impairs regulation of ryanodine receptors from extensor digitorum longus but not soleus muscles.Muscle & nerve · 2018Article
- Skeletal muscle performance and ageing.Journal of cachexia, sarcopenia and muscle · 2018Review
- Rejuvenation of the aged neuromuscular junction by exercise.Cell stress · 2018Review
- The voltage sensor of excitation-contraction coupling in mammals: Inactivation and interaction with CaThe Journal of general physiology · 2017Article
- Transport of the alpha subunit of the voltage gated L-type calcium channel through the sarcoplasmic reticulum occurs prior to localization to triads and requires the beta subunit but not Stac3 in skeletal muscles.Traffic (Copenhagen, Denmark) · 2017Article
- Age-induced oxidative stress: how does it influence skeletal muscle quantity and quality?Journal of applied physiology (Bethesda, Md. : 1985) · 2016Review
- Resistance Training Enhances Skeletal Muscle Innervation Without Modifying the Number of Satellite Cells or their Myofiber Association in Obese Older Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2016Article
- Age-associated repression of type 1 inositol 1, 4, 5-triphosphate receptor impairs muscle regeneration.Aging · 2016Article
- Calpain inhibition rescues troponin T3 fragmentation, increases Cav1.1, and enhances skeletal muscle force in aging sedentary mice.Aging cell · 2016Article
- Ca(2+) leakage out of the sarcoplasmic reticulum is increased in type I skeletal muscle fibres in aged humans.The Journal of physiology · 2016Article
- Age-dependent uncoupling of mitochondria from Ca2⁺ release units in skeletal muscle.Oncotarget · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
In this work we tested the hypothesis that skeletal muscle fibers from aging mice exhibit a significant decline in myoplasmic Ca(2+) concentration resulting from a reduction in L-type Ca(2+) channel (dihydropyridine receptor, DHPR) charge movement. Skeletal muscle fibers from the flexor digitorum brevis (FDB) muscle were obtained from 5-7-, 14-18-, or 21-24-month-old FVB mice and voltage-clamped in the whole-cell configuration of the patch-clamp technique according to described procedures (Wang, Z.-M., M. L. Messi, and O. Delbono. 1999. Biophys. J. 77:2709-2716). Total charge movement or the DHPR charge movement was measured simultaneously with intracellular Ca(2+) concentration. The maximum charge movement (Q(max)) recorded (mean +/- SEM, in nC microF(-1)) was 53 +/- 3.2 (n = 47), 51 +/- 3.2 (n = 35) (non-significant, ns), and 33 +/- 1.9 (n = 32) (p < 0.01), for the three age groups, respectively. Q(max) corresponding to the DHPR was 43 +/- 3.3, 38 +/- 4.1 (ns), and 25 +/- 3.4 (p < 0.01) for the three age groups, respectively. The peak intracellular [Ca(2+)] recorded at 40 mV (in microM) was 15.7 +/- 0. 12, 16.7 +/- 0.18 (ns), and 8.2 +/- 0.07 (p < 0.01) for the three age groups, respectively. No significant changes in the voltage distribution or steepness of the Q-V or [Ca(2+)]-V relationship were found. These data support the concept that the reduction in the peak intracellular [Ca(2+)] results from a larger number of ryanodine receptors uncoupled to DHPRs in skeletal muscle fibers from aging mammals.
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