ArticleBiophysical journal2007
Subunit dependence of Na channel slow inactivation and open channel block in cerebellar neurons.
Article in Biophysical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 50 citations in OpenAlex.
- 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
- Differential Inhibition of Human Nav1.2 Resurgent and Persistent Sodium Currents by Cannabidiol and GS967.International journal of molecular sciences · 2020Article
- Effects of FGF14 and NaThe Journal of general physiology · 2019Article
- Tetrodotoxin-Sensitive Sodium Channels Mediate Action Potential Firing and Excitability in Menthol-Sensitive Vglut3-Lineage Sensory Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Role of sodium channel subtype in action potential generation by neocortical pyramidal neurons.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Need for Speed and Precision: Structural and Functional Specialization in the Cochlear Nucleus of the Avian Auditory System.Journal of experimental neuroscience · 2018Review
- Ionic Mechanism Underlying Rebound Depolarization in Medial Prefrontal Cortex Pyramidal Neurons.Frontiers in cellular neuroscience · 2018Article
- Loss of Navβ4-Mediated Regulation of Sodium Currents in Adult Purkinje Neurons Disrupts Firing and Impairs Motor Coordination and Balance.Cell reports · 2017Article
- Article
- Amyloid precursor protein enhances Nav1.6 sodium channel cell surface expression.The Journal of biological chemistry · 2015Article
- Article
- 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
- Tetrodotoxin-resistant sodium channels in sensory neurons generate slow resurgent currents that are enhanced by inflammatory mediators.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Sodium channel SCN8A (Nav1.6): properties and de novo mutations in epileptic encephalopathy and intellectual disability.Frontiers in genetics · 2013Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Purkinje and cerebellar nuclear neurons both have Na currents with resurgent kinetics. Previous observations, however, suggest that their Na channels differ in their susceptibility to entering long-lived inactivated states. To compare fast inactivation, slow inactivation, and open-channel block, we recorded voltage-clamped, tetrodotoxin-sensitive Na currents in Purkinje and nuclear neurons acutely isolated from mouse cerebellum. In nuclear neurons, recovery from all inactivated states was slower, and open-channel unblock was less voltage-dependent than in Purkinje cells. To test whether specific subunits contributed to this differential stability of inactivation, experiments were repeated in Na(V)1.6-null (med) mice. In med Purkinje cells, recovery times were prolonged and the voltage dependence of open-channel block was reduced relative to control cells, suggesting that availability of Na(V)1.6 is quickly restored at negative potentials. In med nuclear cells, however, currents were unchanged, suggesting that Na(V)1.6 contributes little to wild-type nuclear cells. Extracellular Na(+) prevented slow inactivation more effectively in Purkinje than in nuclear neurons, consistent with a resilience of Na(V)1.6 to slow inactivation. The tendency of nuclear Na channels to inactivate produced a low availability during trains of spike-like depolarization. Hyperpolarizations that approximated synaptic inhibition effectively recovered channels, suggesting that increases in Na channel availability promote rebound firing after inhibition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.