ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Inwardly permeating Na ions generate the voltage dependence of resurgent Na current in cerebellar Purkinje neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 26 citations in OpenAlex.
- Effects of open-channel blocking peptides in NaBiophysical journal · 2025Article
- A Reinterpretation of the Relationship between Persistent and Resurgent Sodium Currents.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Resurgent current in context: Insights from the structure and function of Na and K channels.Biophysical journal · 2024Review
- A Reinterpretation of the Relationship Between Persistent and Resurgent Sodium Currents.bioRxiv : the preprint server for biology · 2024Article
- The Hodgkin-Huxley-Katz Prize Lecture: A Markov model with permeation-dependent gating that accounts for resurgent current of voltage-gated Na channels.The Journal of physiology · 2023Article
- Article
- Resurgent Sodium Current in Neurons of the Cerebral Cortex.Frontiers in cellular neuroscience · 2021Article
- Effects of FGF14 and NaThe Journal of general physiology · 2019Article
- FHF2 isoforms differentially regulate Nav1.6-mediated resurgent sodium currents in dorsal root ganglion neurons.Pflugers Archiv : European journal of physiology · 2017Article
- Navβ4 regulates fast resurgent sodium currents and excitability in sensory neurons.Molecular pain · 2015Article
- Fast-onset long-term open-state block of sodium channels by A-type FHFs mediates classical spike accommodation in hippocampal pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Resurgent current of voltage-gated Na(+) channels.The Journal of physiology · 2014Review
- Interactions among DIV voltage-sensor movement, fast inactivation, and resurgent Na current induced by the NaVβ4 open-channel blocking peptide.The Journal of general physiology · 2013Article
- Antagonism of lidocaine inhibition by open-channel blockers that generate resurgent Na current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- The Hodgkin-Huxley heritage: from channels to circuits.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Review
- The cellular building blocks of breathing.Comprehensive Physiology · 2012Review
- Article
- Anticancer drug oxaliplatin induces acute cooling-aggravated neuropathy via sodium channel subtype Na(V)1.6-resurgent and persistent current.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Voltage-gated sodium channel-associated proteins and alternative mechanisms of inactivation and block.Cellular and molecular life sciences : CMLS · 2012Review
- Cross-species conservation of open-channel block by Na channel β4 peptides reveals structural features required for resurgent Na current.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
Abstract
Voltage-gated Na channels of cerebellar Purkinje neurons express an endogenous open-channel blocking protein. This blocker binds channels at positive potentials and unbinds at negative potentials, generating a resurgent Na current and permitting rapid firing. The macroscopic voltage dependence of resurgent current raises the question of whether the blocker directly senses membrane potential or whether voltage dependence is conferred indirectly. Because we previously found that inwardly permeating Na ions facilitate dissociation of the blocker, we measured voltage-clamped currents in different Na gradients to test the role of permeating ions in generating the voltage dependence of unblock. In reverse gradients, outward resurgent currents were tiny or absent, suggesting that unblock normally requires "knockoff" by Na. Inward resurgent currents at strongly negative potentials, however, were larger in reverse than in control gradients. Moreover, occupancy of the blocked state was prolonged both in reverse gradients and in control gradients with reduced Na concentrations, indicating that block is more stable when inward currents are small. Accordingly, reverse gradients shifted the voltage dependence of block, such that resurgent currents were evoked even after conditioning at negative potentials. Additionally, in control gradients, peak resurgent currents decreased linearly with driving force during the conditioning step, suggesting that the stability of block varies directly with inward Na current amplitude. Thus, the voltage dependence of blocker unbinding results almost entirely from repulsion by Na ions occupying the external pore. The lack of voltage sensitivity of the blocking protein suggests that the blocker's binding site lies outside the membrane field, in the permeation pathway.
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