ArticleExperimental brain research2006
Upregulation of persistent and ramp sodium current in dorsal horn neurons after spinal cord injury.
Article in Experimental brain research, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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Who cites it
49 citing papers in PubMed, 101 citations in OpenAlex.
- Targeting Spinal Dorsal Horn Sensitisation in Chronic Pain: Mechanisms and Translational Strategies.Neuroscience bulletin · 2026Review
- Sevoflurane inhibition of the developmentally expressed neuronal sodium channel NaScientific reports · 2025Article
- Nociceptor sodium channels shape subthreshold phase, upstroke, and shoulder of action potentials.The Journal of general physiology · 2025Article
- Article
- Comparative outcomes of microsurgical dorsal root entry zone lesioning (DREZotomy) for intractable neuropathic pain in spinal cord and cauda equina injuries.Neurosurgical review · 2025Article
- An electrophysiologist's guide to dorsal horn excitability and pain.Frontiers in cellular neuroscience · 2025Review
- Spinal Cord Stimulation for Spinal Cord Injury-Related Pain: A Pilot Study.Brain sciences · 2024Article
- Cold and warmth intensify pain-linked sodium channel gating effects and persistent currents.The Journal of general physiology · 2023Article
- SCN8A epileptic encephalopathy mutations display a gain-of-function phenotype and divergent sensitivity to antiepileptic drugs.Acta pharmacologica Sinica · 2022Article
- The Molecular Basis and Pathophysiology of Trigeminal Neuralgia.International journal of molecular sciences · 2022Review
- Molecular Mechanisms of Astaxanthin as a Potential Neurotherapeutic Agent.Marine drugs · 2021Review
- Regional Hyperexcitability and Chronic Neuropathic Pain Following Spinal Cord Injury.Cellular and molecular neurobiology · 2020Review
- The Neuroprotective Effects of Astaxanthin: Therapeutic Targets and Clinical Perspective.Molecules (Basel, Switzerland) · 2019Review
- Addressing the Issue of Tetrodotoxin Targeting.Marine drugs · 2018Review
- Sodium Channel SCN3A (NaNeuron · 2018Article
- Mutations in SCN3A cause early infantile epileptic encephalopathy.Annals of neurology · 2018Article
- Ionic Homeostasis Maintenance in ALS: Focus on New Therapeutic Targets.Frontiers in neuroscience · 2018Review
- Distribution and function of voltage-gated sodium channels in the nervous system.Channels (Austin, Tex.) · 2017Review
- Opposite, bidirectional shifts in excitation and inhibition in specific types of dorsal horn interneurons are associated with spasticity and pain post-SCI.Scientific reports · 2017Article
- Acute cocaine exposure elicits rises in calcium in arousal-related laterodorsal tegmental neurons.Pharmacology research & perspectives · 2017Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Traumatic spinal cord injury (SCI) results not only in motor impairment, but also in chronic central neuropathic pain, which often is refractory to conventional treatment approaches. Upregulated expression of sodium channel Nav1.3 has been observed within the spinal dorsal horn neurons after SCI, and appears to contribute to neuronal hyperresponsiveness and pain-related behaviors. In this study we characterized the changes in sodium current properties within dorsal horn neurons after contusive SCI. Four weeks after adult male Sprague-Dawley rats underwent T9 spinal cord contusion injury, when behavioral nociceptive thresholds were decreased to both mechanical and thermal stimuli, whole-cell patch-clamp recordings were performed on acutely dissociated lumbar dorsal horn neurons. The cells demonstrated characteristic fast-activating and fast-inactivating sodium currents. SCI led to a shift of the steady-state activation and inactivation of the sodium current towards more depolarized potentials. The shifted steady-state inactivation shows similarities to that obtained from axotomized dorsal root ganglions, which were shown to upregulate Nav1.3. Small slow depolarizations below action potential threshold produced ramp currents, which were markedly enhanced by SCI (from 182 +/- 41 to 338 +/- 55 pA). The density of the noninactivating persistent sodium current was also significantly enhanced in neurons from SCI animals (from 17.4 +/- 3.2 to 27.7 +/- 4.4 pA/pF at 50-70 ms of depolarization). The increased persistent sodium current and ramp current, which are consistent with upregulation of Nav1.3 within dorsal horn neurons, suggest a basis for the hyperresponsiveness of these neurons following SCI.
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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.