ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Developmental expression of the TTX-resistant voltage-gated sodium channels Nav1.8 (SNS) and Nav1.9 (SNS2) in primary sensory neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
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Who cites it
68 citing papers in PubMed, 156 citations in OpenAlex.
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- NCX2 Targeting as a Neuroprotective Strategy Against Oxaliplatin-Induced Peripheral Neurotoxicity.Cancers · 2026Article
- Macrophage-secreted brain-derived neurotrophic factor promotes tumor growth in triple-negative breast cancer by inducing axonogenesis.Cell death and differentiation · 2026Article
- Targeting Supramolecular Active Complexes of NaAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Astrocyte Store-Released Calcium Modulates Visual Cortex Synapse Development and Circuit Function.Research square · 2025Article
- The maturation of spinal dorsal horn nociceptive neuronal network activity over the postnatal period.Pain reports · 2025Article
- Modulation of Voltage-Gated Sodium Channels from Sensory Neurons by Isoeugenol.International journal of molecular sciences · 2025Article
- Nav1.8 and Chronic Pain: From Laboratory Animals to Clinical Patients.Biomolecules · 2025Review
- mRNA Expression of Mineralocorticoid and Glucocorticoid Receptors in Human and Mouse Sensory Neurons of the Dorsal Root Ganglia.Anesthesia and analgesia · 2025Article
- Schwann cell-secreted PGECell · 2024Article
- Genetic Analysis ofInternational journal of molecular sciences · 2024Article
- The influence of Nav1.9 channels on intestinal hyperpathia and dysmotility.Channels (Austin, Tex.) · 2023Review
- Brugada Syndrome: From Molecular Mechanisms and Genetics to Risk Stratification.International journal of molecular sciences · 2023Review
- Obesity-Associated Neuropathy: Recent Preclinical Studies and Proposed Mechanisms.Antioxidants & redox signaling · 2022Review
- The impact of C-tactile low-threshold mechanoreceptors on affective touch and social interactions in mice.Science advances · 2022Article
- Transiently Nav1.8-expressing neurons are capable of sensing noxious stimuli in the brain.Frontiers in cellular neuroscience · 2022Article
- The development of somatosensory neurons: Insights into pain and itch.Current topics in developmental biology · 2021Review
- Regulation of Ion Channel Function by Gas Molecules.Advances in experimental medicine and biology · 2021Review
- Carvedilol Exerts Neuroprotective Effect on Rat Model of Diabetic Neuropathy.Frontiers in pharmacology · 2021Article
- Article
8 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
The development of neuronal excitability involves the coordinated expression of different voltage-gated ion channels. We have characterized the expression of two sensory neuron-specific tetrodotoxin-resistant sodium channel alpha subunits, Na(v)1. (SNS/PN3) and Na(v)1.9 (SNS2/NaN), in developing rat lumbar dorsal root ganglia (DRGs). Expression of both Na(v)1.8 and Na(v)1.9 increases with age, beginning at embryonic day (E) 15 and E17, respectively, and reaching adult levels by postnatal day 7. Their distribution is restricted mainly to those subpopulations of primary sensory neurons in developing and adult DRGs that give rise to unmyelinated C-fibers (neurofilament 200 negative). Na(v)1.8 is expressed in a higher proportion of neuronal profiles than Na(v)1.9 at all stages during development, as in the adult. At E17, almost all Na(v)1.8-expressing neurons also express the high-affinity NGF receptor TrkA, and only a small proportion bind to IB4, a marker for c-ret-expressing (glial-derived neurotrophic factor-responsive) neurons. Because IB4 binding neurons differentiate from TrkA neurons in the postnatal period, the proportion of Na(v)1.8 cells that bind to IB4 increases, in parallel with a decrease in the proportion of Na(v)1.8-TrkA co-expressing cells. In contrast, an equal number of Na(v)1.9 cells bind IB4 and TrkA in embryonic life. The differential expression of Na(v)1.8 and Na(v)1.9 in late embryonic development, with their distinctive kinetic properties, may contribute to the development of spontaneous and stimulus-evoked excitability in small diameter primary sensory neurons in the perinatal period and the activity-dependent changes in differentiation they produce.
Indexed as
Identifiers
11487631PMC6763192W1590770581What OpenQuestion holds
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.