ReviewThe Journal of physiology2012
Sodium channels, the electrogenisome and the electrogenistat: lessons and questions from the clinic.
Review in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
- Nav1.8 Variant I206M as a Latent Susceptibility Factor in Postaxotomy Ocular Pain.Neurology. Genetics · 2026Article
- High-throughput multiplex voltage-clamp/current-clamp evaluation of acutely isolated neurons.Nature protocols · 2026Review
- Article
- Targeting sodium channels - challenges for acute pain and the leap to chronic pain.Nature reviews. Neurology · 2025Review
- Nav1.8: Intrinsic limits on the functional effect of abrogation in DRG neurons.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Voltage-gated sodium channels in excitable cells as drug targets.Nature reviews. Drug discovery · 2025Review
- Sodium currents in naïve mouse dorsal root ganglion neurons: No major differences between sexes.Channels (Austin, Tex.) · 2024Article
- TRPM8 Mutations Associated With Persistent Pain After Surgical Injury of Corneal Trigeminal Axons.Neurology. Genetics · 2024Article
- Interplay of Nav1.8 and Nav1.7 channels drives neuronal hyperexcitability in neuropathic pain.The Journal of general physiology · 2024Article
- IThe Journal of physiology · 2023Article
- Gene therapy for chronic pain: emerging opportunities in target-rich peripheral nociceptors.Nature reviews. Neuroscience · 2023Review
- Nav1.7 P610T mutation in two siblings with persistent ocular pain after corneal axon transection: impaired slow inactivation and hyperexcitable trigeminal neurons.Journal of neurophysiology · 2023Article
- High-throughput combined voltage-clamp/current-clamp analysis of freshly isolated neurons.Cell reports methods · 2023Article
- Kv7-specific activators hyperpolarize resting membrane potential and modulate human iPSC-derived sensory neuron excitability.Frontiers in pharmacology · 2023Article
- Neural Assemblies as Precursors for Brain Function.NeuroSci · 2022Article
- Voltage-gated sodium channels in diabetic sensory neuropathy: Function, modulation, and therapeutic potential.Frontiers in cellular neuroscience · 2022Review
- Chemometric Models of Differential Amino Acids at the NaMolecules (Basel, Switzerland) · 2020Article
- Membrane cholesterol depletion as a trigger of Nav1.9 channel-mediated inflammatory pain.The EMBO journal · 2018Article
- Primary erythromelalgia: a review.Orphanet journal of rare diseases · 2015Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In the six decades that have followed the work of Hodgkin and Huxley, multiple generations of neuroscientists and biophysicists have built upon their pivotal contributions. It is now clear that, in mammals, nine genes encode nine distinct voltage-gated sodium channels with different amino acid sequences and different physiological and pharmacological properties. The different sodium channel isoforms produce a multiplicity of distinct sodium currents with different time-dependent characteristics and voltage dependencies, which interact with each other and with the currents produced by other channels (including calcium and potassium channels) to shape neuronal firing patterns. Expression of these sodium channel isoforms is highly dynamic, both in the normal nervous system, and in the injured nervous system. Recent research has shed light on the roles of sodium channels in human disease, a development that may open up new therapeutic strategies. This article examines the pain-signalling system as an example of a neuronal network where multiple sodium channel isoforms play complementary roles in electrogenesis and a strong link with human disease has been established. Recent research suggests that it may be possible to target specific sodium channel isoforms that drive hyperexcitability in pain-signalling neurons, thereby providing new therapeutic strategies for chronic pain, and providing an illustration of the impact of the Hodgkin-Huxley legacy in the clinical domain.
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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.