ArticleThe Journal of general physiology2008
Ni2+ block of CaV3.1 (alpha1G) T-type calcium channels.
Article in The Journal of general physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed.
- Differential contribution of T-type voltage-gated calcium channels to vascular reactivity in the aorta and renal artery of healthy rabbits.Experimental physiology · 2026Article
- Enniatins A1 and B1 Modulate Calcium Flux through Alternative Pathways beyond Mitochondria.Journal of agricultural and food chemistry · 2024Article
- Optogenetic activation of the inhibitory nigro-collicular circuit evokes contralateral orienting movements in mice.Cell reports · 2022Article
- Low-voltage-activated inward current in murine antral smooth muscle cells is an artifact.American journal of physiology. Cell physiology · 2021Article
- Functional Postnatal Maturation of the Medial Olivocochlear Efferent-Outer Hair Cell Synapse.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Functional Specialization of Interneuron Dendrites: Identification of Action Potential Initiation Zone in Axonless Olfactory Bulb Granule Cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The Low-Threshold Calcium Channel Cav3.2 Mediates Burst Firing of Mature Dentate Granule Cells.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- Evolutionary insights into T-type CaThe Journal of general physiology · 2017Article
- Models of calcium permeation through T-type channels.Pflugers Archiv : European journal of physiology · 2014Review
- Complex modulation of Ca(v)3.1 T-type calcium channel by nickel.Cellular and molecular life sciences : CMLS · 2013Article
- Fe²⁺ block and permeation of CaV3.1 (α1G) T-type calcium channels: candidate mechanism for non-transferrin-mediated Fe²⁺ influx.Molecular pharmacology · 2012Article
- Epigallocatechin-3-gallate induces mesothelioma cell death via H2 O2 -dependent T-type Ca2+ channel opening.Journal of cellular and molecular medicine · 2012Article
- Calcium microdomains near R-type calcium channels control the induction of presynaptic long-term potentiation at parallel fiber to purkinje cell synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Article
- Evaluation of a two-site, three-barrier model for permeation in Ca(V)3.1 (alpha1G) T-type calcium channels: Ca (2+), Ba (2+), Mg (2+), and Na (+).The Journal of membrane biology · 2010Article
- A malignant hyperthermia-inducing mutation in RYR1 (R163C): alterations in Ca2+ entry, release, and retrograde signaling to the DHPR.The Journal of general physiology · 2010Article
- Transient and big are key features of an invertebrate T-type channel (LCav3) from the central nervous system of Lymnaea stagnalis.The Journal of biological chemistry · 2010Article
- Permeation and gating in CaV3.1 (alpha1G) T-type calcium channels effects of Ca2+, Ba2+, Mg2+, and Na+.The Journal of general physiology · 2008Article
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Authors and funding
3 authors.
Funding
Abstract
Ni(2+) inhibits current through calcium channels, in part by blocking the pore, but Ni(2+) may also allosterically affect channel activity via sites outside the permeation pathway. As a test for pore blockade, we examined whether the effect of Ni(2+) on Ca(V)3.1 is affected by permeant ions. We find two components to block by Ni(2+), a rapid block with little voltage dependence, and a slow block most visible as accelerated tail currents. Rapid block is weaker for outward vs. inward currents (apparent K(d) = 3 vs. 1 mM Ni(2+), with 2 mM Ca(2+) or Ba(2+)) and is reduced at high permeant ion concentration (110 vs. 2 mM Ca(2+) or Ba(2+)). Slow block depends both on the concentration and on the identity of the permeant ion (Ca(2+) vs. Ba(2+) vs. Na(+)). Slow block is 2-3x faster in Ba(2+) than in Ca(2+) (2 or 110 mM), and is approximately 10x faster with 2 vs. 110 mM Ca(2+) or Ba(2+). Slow block is orders of magnitude slower than the diffusion limit, except in the nominal absence of divalent cations ( approximately 3 muM Ca(2+)). We conclude that both fast and slow block of Ca(V)3.1 by Ni(2+) are most consistent with occlusion of the pore. The exit rate of Ni(2+) for slow block is reduced at high Ni(2+) concentrations, suggesting that the site responsible for fast block can "lock in" slow block by Ni(2+), at a site located deeper within the pore. In contrast to the complex pore block observed for Ca(V)3.1, inhibition of Ca(V)3.2 by Ni(2+) was essentially independent of voltage, and was similar in 2 mM Ca(2+) vs. Ba(2+), consistent with inhibition by a different mechanism, at a site outside the pore.
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Registered trials
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