ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Persistent sodium current in layer 5 neocortical neurons is primarily generated in the proximal axon.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers, 1 of them a synthesis that pooled it.
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Who cites it
60 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.
- Persistent sodium currents in neurons: potential mechanisms and pharmacological blockers.Pflugers Archiv : European journal of physiology · 2024Pooled it
- Capsaicin and menthol reduce excitability of insular pyramidal neurons via TRP-independent sodium channel inactivation.Experimental brain research · 2026Article
- Axon initial segment structure and function in health and disease.Physiological reviews · 2025Review
- Nodal NaFrontiers in cellular neuroscience · 2025Article
- Analysis of the effect of the scorpion toxin AaH-II on action potential generation in the axon initial segment.Scientific reports · 2024Article
- SUMOylation of NaeLife · 2023Article
- The M-current works in tandem with the persistent sodium current to set the speed of locomotion.PLoS biology · 2020Article
- Isoflurane Modulates Hippocampal Cornu Ammonis Pyramidal Neuron Excitability by Inhibition of Both Transient and Persistent Sodium Currents in Mice.Anesthesiology · 2019Article
- The MAP1B Binding Domain of NaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Alterations of Electrophysiological Properties and Ion Channel Expression in Prefrontal Cortex of a Mouse Model of Schizophrenia.Frontiers in cellular neuroscience · 2019Article
- Axonal Computations.Frontiers in cellular neuroscience · 2019Review
- Neuromodulation of Axon Terminals.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- 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
- Article
- Voltage-Gated Sodium Channels in Neocortical Pyramidal Neurons Display Cole-Moore Activation Kinetics.Frontiers in cellular neuroscience · 2018Article
- The modulation of two motor behaviors by persistent sodium currents inJournal of neurophysiology · 2017Article
- Is realistic neuronal modeling realistic?Journal of neurophysiology · 2016Review
- Increased Persistent Sodium Current Causes Neuronal Hyperexcitability in the Entorhinal Cortex of Fmr1 Knockout Mice.Cell reports · 2016Article
- Single-Molecule Imaging of Nav1.6 on the Surface of Hippocampal Neurons Reveals Somatic Nanoclusters.Biophysical journal · 2016Article
- Ionic mechanisms maintaining action potential conduction velocity at high firing frequencies in an unmyelinated axon.Physiological reports · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In addition to the well described fast-inactivating component of the Na+ current [transient Na+ current (INaT)], neocortical neurons also exhibit a low-voltage-activated, slowly inactivating "persistent" Na+ current (INaP), which plays a role in determining neuronal excitability and synaptic integration. We investigated the Na+ channels responsible for INaP in layer 5 pyramidal cells using cell-attached and whole-cell recordings in neocortical slices. In simultaneous cell-attached and whole-cell somatic recordings, no persistent Na+ channel activity was detected at potentials at which whole-cell INaP operates. Detailed kinetic analysis of late Na+ channel activity in cell-attached patches at 36 degrees C revealed that somatic Na+ channels do not demonstrate "modal gating" behavior and that the probability of single late openings is extremely low (<1.4 x 10(-4) or <0.02% of maximal open probability of INaT). Ensemble averages of these currents did not reveal a sustained component whose amplitude and voltage dependence could account for INaP as seen in whole-cell recordings. Local application of TTX to the axon blocked somatically recorded INaP, whereas somatic and dendritic application had little or no effect. Finally, simultaneous current-clamp recordings from soma and apical dendrite revealed that Na+ plateau potentials originate closer to the axon. Our data indicate that the primary source of INaP is in the spike initiation zone in the proximal axon. The focal axonal presence of regenerative subthreshold conductance with voltage and time dependence optimal to manipulate integration of synaptic input, spike threshold, and the pattern of repetitive firing provides the layer 5 pyramidal neuron with a mechanism for dynamic control of its gain.
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