ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006
Impaired firing and cell-specific compensation in neurons lacking nav1.6 sodium channels.
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 90 papers.
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Who cites it
90 citing papers in PubMed, 135 citations in OpenAlex.
- Intrinsic electrical diversity of PViScience · 2026Article
- Compensatory rearrangement of parvalbumin interneuron voltage-gated sodium channel subunits in a mouse model of Dravet syndrome.Epilepsia · 2026Article
- Ectopic sodium channel expression decreases excitability of Drosophila Kenyon cells.The Journal of physiology · 2025Article
- Astrocyte-induced firing in primary afferent axons.iScience · 2025Article
- Differential Intrinsic Firing Properties in Sustained and Transient Mouse αRGCs Match Their Light Response Characteristics and Persist during Retinal Degeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Voltage-Gated Ion Channel Compensatory Effect in DEE: Implications for Future Therapies.Cells · 2024Review
- Crosstalk among WEE1 Kinase, AKT, and GSK3 in Nav1.2 Channelosome Regulation.International journal of molecular sciences · 2024Article
- Experimental and computational evidence that Calpain-10 binds to the carboxy terminus of NaScientific reports · 2024Article
- Characterization of NaLife science alliance · 2024Article
- [Expression changes of NaNan fang yi ke da xue xue bao = Journal of Southern Medical University · 2023Article
- Microfluidic Platforms Promote Polarization of Human-Derived Retinal Ganglion Cells That Model Axonopathy.Translational vision science & technology · 2023Article
- Cryo-EM structure of human voltage-gated sodium channel NaProceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Biophysical KeLife · 2022Article
- Review
- Inhibition of the Akt/PKB Kinase Increases NaInternational journal of molecular sciences · 2022Article
- An emerging spectrum of variants and clinical features inChannels (Austin, Tex.) · 2021Review
- Morphological Factors that Underlie Neural Sensitivity to Stimulation in the Retina.Advanced nanobiomed research · 2021Article
- Resurgent NaNature communications · 2021Article
- Sodium channelopathies of skeletal muscle and brain.Physiological reviews · 2021Review
30 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability of neurons to fire precise patterns of action potentials is critical for encoding inputs and efficiently driving target neurons. At the axon initial segment and nodes of Ranvier, where nerve impulses are generated and propagated, a high density of Na(v)1.2 sodium channels is developmentally replaced by Na(v)1.6 channels. In retinal ganglion cells (GCs), this isoform switch coincides with the developmental transition from single spikes to repetitive firing. Also, Na(v)1.6 channels are required for repetitive spiking in cerebellar Purkinje neurons. These previous observations suggest that the developmental appearance of Na(v)1.6 underlies the transition to repetitive spiking in GCs. To test this possibility, we recorded from GCs of med (Na(v)1.6-null) and wild-type mice during postnatal development. By postnatal day 18, when the switch to Na(v)1.6 at GC initial segments is normally complete, the maximal sustained and instantaneous firing rates were lower in med than in wild-type GCs, demonstrating that Na(v)1.6 channels are necessary to attain physiologically relevant firing frequencies in GCs. However, the firing impairment was milder than that reported previously in med Purkinje neurons, which prompted us to look for differences in compensatory sodium channel expression. Both Na(v)1.2 and Na(v)1.1 channels accumulated at initial segments and nodes of med GCs, sites normally occupied by Na(v)1.6. In med Purkinje cells, only Na(v)1.1 channels were found at initial segments, whereas in other brain regions, only Na(v)1.2 was detected at med initial segments and nodes. Thus, compensatory mechanisms in channel isoform distribution are cell specific, which likely results in different firing properties.
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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.