ArticleThe Journal of general physiology2004
Influence of permeant ions on voltage sensor function in the Kv2.1 potassium channel.
Article in The Journal of general physiology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Electric field-induced pore constriction in the human KProceedings of the National Academy of Sciences of the United States of America · 2025Article
- The tarantula toxin GxTx detains KThe Journal of general physiology · 2019Article
- Interaction of the S6 proline hinge with N-type and C-type inactivation in Kv1.4 channels.Biophysical journal · 2012Article
- Action potentials in primary osteoblasts and in the MG-63 osteoblast-like cell line.Journal of bioenergetics and biomembranes · 2011Article
- The binding of donepezil with external mouth of K+-channels of molluscan neurons.Cellular and molecular neurobiology · 2009Article
- Atypical gating of M-type potassium channels conferred by mutations in uncharged residues in the S4 region of KCNQ2 causing benign familial neonatal convulsions.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
- Control of single channel conductance in the outer vestibule of the Kv2.1 potassium channel.The Journal of general physiology · 2006Article
- Modulation of Kv2.1 channel gating and TEA sensitivity by distinct domains of SNAP-25.The Biochemical journal · 2006Article
- Relationship between pore occupancy and gating in BK potassium channels.The Journal of general physiology · 2006Article
Corrections and comments
- Erratum issued
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
We previously demonstrated that the outer vestibule of activated Kv2.1 potassium channels can be in one of two conformations, and that K(+) occupancy of a specific selectivity filter site determines which conformation the outer vestibule is in. These different outer vestibule conformations result in different sensitivities to internal and external TEA, different inactivation rates, and different macroscopic conductances. The [K(+)]-dependent switch in outer vestibule conformation is also associated with a change in rate of channel activation. In this paper, we examined the mechanism by which changes in [K(+)] modulate the rate of channel activation. Elevation of symmetrical [K(+)] or [Rb(+)] from 0 to 3 mM doubled the rate of on-gating charge movement (Q(on)), measured at 0 mV. Cs(+) produced an identical effect, but required 40-fold higher concentrations. All three permeant ions occupied the selectivity filter over the 0.03-3 mM range, so simple occupancy of the selectivity filter was not sufficient to produce the change in Q(on). However, for each of these permeant ions, the speeding of Q(on) occurred with the same concentration dependence as the switch between outer vestibule conformations. Neutralization of an amino acid (K356) in the outer vestibule, which abolishes the modulation of channel pharmacology and ionic currents by the K(+)-dependent reorientation of the outer vestibule, also abolished the K(+)-dependence of Q(on). Together, the data indicate that the K(+)-dependent reorientation in the outer vestibule was responsible for the change in Q(on). Moreover, similar [K(+)]-dependence and effects of mutagenesis indicate that the K(+)-dependent change in rate of Q(on) can account for the modulation of ionic current activation rate. Simple kinetic analysis suggested that K(+) reduced an energy barrier for voltage sensor movement. These results provide strong evidence for a direct functional interaction, which is modulated by permeant ions acting at the selectivity filter, between the outer vestibule of the Kv2.1 potassium channel and the voltage sensor.
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