ArticleBiophysical journal1999
N-type calcium channel inactivation probed by gating-current analysis.
Article in Biophysical journal, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 58 citations in OpenAlex.
- Inactivation of CaV1 and CaV2 channels.The Journal of general physiology · 2025Review
- Constitutive activity of dopamine receptor type 1 (D1R) increases CaV2.2 currents in PFC neurons.The Journal of general physiology · 2020Article
- Allosteric regulators selectively prevent CaeLife · 2018Article
- Fast Inactivation of CaJournal of molecular neuroscience : MN · 2017Article
- Contrasting the roles of the I-II loop gating brake in CaV3.1 and CaV3.3 calcium channels.Pflugers Archiv : European journal of physiology · 2015Article
- From foe to friend: using animal toxins to investigate ion channel function.Journal of molecular biology · 2015Review
- The tetramerization domain potentiates Kv4 channel function by suppressing closed-state inactivation.Biophysical journal · 2014Article
- Tetraspanin-13 modulates voltage-gated CaV2.2 Ca2+ channels.Scientific reports · 2013Article
- Nanodomain Ca²⁺ of Ca²⁺ channels detected by a tethered genetically encoded Ca²⁺ sensor.Nature communications · 2012Article
- Mechanisms of closed-state inactivation in voltage-gated ion channels.The Journal of physiology · 2011Review
- Systematic mapping of the state dependence of voltage- and Ca2+-dependent inactivation using simple open-channel measurements.The Journal of general physiology · 2010Article
- Molecular endpoints of Ca2+/calmodulin- and voltage-dependent inactivation of Ca(v)1.3 channels.The Journal of general physiology · 2010Article
- Open-state occupancy prevents gating charge relaxation of N-type (CaV2.2) calcium channels.Biophysical journal · 2009Article
- Crystal structure of the CaV2 IQ domain in complex with Ca2+/calmodulin: high-resolution mechanistic implications for channel regulation by Ca2+.Structure (London, England : 1993) · 2008Article
- Gating charge immobilization in Kv4.2 channels: the basis of closed-state inactivation.The Journal of general physiology · 2008Article
- Role of N-terminal domain and accessory subunits in controlling deactivation-inactivation coupling of Kv4.2 channels.Biophysical journal · 2008Article
- The Timothy syndrome mutation differentially affects voltage- and calcium-dependent inactivation of CaV1.2 L-type calcium channels.Proceedings of the National Academy of Sciences of the United States of America · 2008Article
- Schwann cell-derived factors modulate synaptic activities at developing neuromuscular synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Differential regulation of endogenous N- and P/Q-type Ca2+ channel inactivation by Ca2+/calmodulin impacts on their ability to support exocytosis in chromaffin cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Elementary mechanisms producing facilitation of Cav2.1 (P/Q-type) channels.The Journal of general physiology · 2007Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-type calcium channels inactivate most rapidly in response to moderate, not extreme depolarization. This behavior reflects an inactivation rate that bears a U-shaped dependence on voltage. Despite this apparent similarity to calcium-dependent inactivation, N-type channel inactivation is insensitive to the identity of divalent charge carrier and, in some reports, to the level of internal buffering of divalent cations. Hence, the inactivation of N-type channels fits poorly with the "classic" profile for either voltage-dependent or calcium-dependent inactivation. To investigate this unusual inactivation behavior, we expressed recombinant N-type calcium channels in mammalian HEK 293 cells, permitting in-depth correlation of ionic current inactivation with potential alterations of gating current properties. Such correlative measurements have been particularly useful in distinguishing among various inactivation mechanisms in other voltage-gated channels. Our main results are the following: 1) The degree of gating charge immobilization was unchanged by the block of ionic current and precisely matched by the extent of ionic current inactivation. These results argue for a purely voltage-dependent mechanism of inactivation. 2) The inactivation rate was fastest at a voltage where only approximately (1)/(3) of the total gating charge had moved. This unusual experimental finding implies that inactivation occurs most rapidly from intermediate closed conformations along the activation pathway, as we demonstrate with novel analytic arguments applied to coupled-inactivation schemes. These results provide strong, complementary support for a "preferential closed-state" inactivation mechanism, recently proposed on the basis of ionic current measurements of recombinant N-type channels (Patil et al., . Neuron. 20:1027-1038).
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