ArticleThe Journal of physiology1995
Excessive repolarization-dependent calcium currents induced by strong depolarizations in rat skeletal myoballs.
Article in The Journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 24 citations in OpenAlex.
- Sites of proteolytic processing and noncovalent association of the distal C-terminal domain of CaV1.1 channels in skeletal muscle.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Ca(2+) calmodulin kinase and calcineurin mediate IGF-1-induced skeletal muscle dihydropyridine receptor alpha(1S) transcription.The Journal of membrane biology · 2004Article
- The beta1a subunit regulates the functional properties of adult frog and mouse L-type Ca2+ channels of skeletal muscle.The Journal of physiology · 2002Article
- Voltage- and calcium-dependent inactivation of calcium channels in Lymnaea neurons.The Journal of general physiology · 1999Article
- Insulin-like growth factor-1 enhances rat skeletal muscle charge movement and L-type Ca2+ channel gene expression.The Journal of physiology · 1999Article
- Depolarization-induced slowing of Ca2+ channel deactivation in squid neurons.Biophysical journal · 1997Article
- Modulation of the cloned skeletal muscle L-type Ca2+ channel by anchored cAMP-dependent protein kinase.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- Absence of Ca2+ current facilitation in skeletal muscle of transgenic mice lacking the type 1 ryanodine receptor.The Journal of physiology · 1996Article
- Long Ca2+ channel opening induced by large depolarization and Bay K 8644 in smooth muscle cells isolated from guinea-pig detrusor.British journal of pharmacology · 1996Article
- Silent calcium channels generate excessive tail currents and facilitation of calcium currents in rat skeletal myoballs.The Journal of physiology · 1996Article
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. Whole-cell patch-clamp recordings were used to study voltage-dependent Ca2+ currents in skeletal myoballs cultured from newborn rats. 2. Depolarizing voltage pulses evoked classical L-type Ca2+ currents, whereas repolarization induced tail currents, whose properties deviated from the expected behaviour of the preceding Ca2+ currents in both voltage dependence and kinetics. 3. Depolarizations of up to +10 mV primarily recruited tail currents that correspond to the Ca2+ channels activated and conducting during the depolarizing pulse, but stronger depolarizations yielded an additional tail current component that exceeded the 'normal' tail current amplitude by several-fold. 4. Activation kinetics of the tail currents were biexponential, with a fast time constant matching the activation time course of the pulse currents (tau approximately 40 ms) and an additional slower component with a voltage-dependent time course that had no kinetic counterpart in the pulse currents (tau approximately 150-600 ms). 5. Both pulse and tail currents were blocked by the dihydropyridine, PN200-110, suggesting that they represent Ca2+ channels of the L-type. 6. We suggest the presence of at least two subsets of dihydropyridine-sensitive Ca2+ channels in skeletal muscle cells. One subset has classical L-type channel characteristics and the other has anomalous gating behaviour that is 'activated' or 'primed' by strong and long-lasting depolarizations without conducting significant Ca2+ current--however, upon repolarization, this subset of channels generates large tail currents.
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