ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2001
Glycosylation alters steady-state inactivation of sodium channel Nav1.9/NaN in dorsal root ganglion neurons and is developmentally regulated.
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 49 papers.
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The trial behind it
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Who cites it
49 citing papers in PubMed, 105 citations in OpenAlex.
- Infantile Pain Episodes Associated with Novel Nav1.9 Mutations in Familial Episodic Pain Syndrome in Japanese Families.PloS one · 2016Trial
- The response to anti-seizure medications and the development of pharmacoresistant epilepsy in malformations of cortical development.BMC medicine · 2025Article
- Discovery of E0199: A novel compound targeting both peripheral NaJournal of pharmaceutical analysis · 2025Article
- Genetic Analysis ofInternational journal of molecular sciences · 2024Article
- The Mechanisms of Plasticity of Nociceptive Ion Channels in Painful Diabetic Neuropathy.Frontiers in pain research (Lausanne, Switzerland) · 2022Review
- Contributions of NaScientific reports · 2021Article
- Review
- Glycosylation of β1 subunit plays a pivotal role in the toxin sensitivity and activation of BK channels.The journal of venomous animals and toxins including tropical diseases · 2021Article
- SCN11A gene deletion causes sensorineural hearing loss by impairing the ribbon synapses and auditory nerves.BMC neuroscience · 2021Article
- Mechanisms Underlying Gastrodin Alleviating Vincristine-Induced Peripheral Neuropathic Pain.Frontiers in pharmacology · 2021Article
- Glycosylation of CaFrontiers in cellular neuroscience · 2020Article
- Sensitization of TRPV1 receptors by TNF-α orchestrates the development of vincristine-induced pain.Oncology letters · 2018Article
- Article
- N-glycan content modulates kainate receptor functional properties.The Journal of physiology · 2017Article
- Stromal Cell-Derived Factor 1 Increases Tetrodotoxin-Resistant Sodium Currents Nav1.8 and Nav1.9 in Rat Dorsal Root Ganglion Neurons via Different Mechanisms.Neurochemical research · 2016Article
- Voltage-Gated Na+ Channels: Not Just for Conduction.Cold Spring Harbor perspectives in biology · 2016Review
- Single amino acid deletion in transmembrane segment D4S6 of sodium channel Scn8a (Nav1.6) in a mouse mutant with a chronic movement disorder.Neurobiology of disease · 2016Article
- Direct Current-Induced Calcium Trafficking in Different Neuronal Preparations.Neural plasticity · 2016Article
- Painful Diabetic Neuropathy: Prevention or Suppression?International review of neurobiology · 2016Review
- Sialic acids attached to N- and O-glycans within the Nav1.4 D1S5-S6 linker contribute to channel gating.Biochimica et biophysica acta · 2015Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Na channel NaN (Na(v)1.9) produces a persistent TTX-resistant (TTX-R) current in small-diameter neurons of dorsal root ganglia (DRG) and trigeminal ganglia. Na(v)1.9-specific antibodies react in immunoblot assays with a 210 kDa protein from the membrane fractions of adult DRG and trigeminal ganglia. The size of the immunoreactive protein is in close agreement with the predicted Na(v)1.9 theoretical molecular weight of 201 kDa, suggesting limited glycosylation of this channel in adult tissues. Neonatal rat DRG membrane fractions, however, contain an additional higher molecular weight immunoreactive protein. Reverse transcription-PCR analysis did not show additional longer transcripts that could encode the larger protein. Enzymatic deglycosylation of the membrane preparations converted both immunoreactive proteins into a single faster migrating band, consistent with two states of glycosylation of Na(v)1.9. The developmental change in the glycosylation state of Na(v)1.9 is paralleled by a developmental change in the gating of the persistent TTX-R Na(+) current attributable to Na(v)1.9 in native DRG neurons. Whole-cell patch-clamp analysis demonstrates that the midpoint of steady-state inactivation is shifted 7 mV in a hyperpolarized direction in neonatal (postnatal days 0-3) compared with adult DRG neurons, although there is no significant difference in activation. Pretreatment of neonatal DRG neurons with neuraminidase causes an 8 mV depolarizing shift in the midpoint of steady-state inactivation of Na(v)1.9, making it indistinguishable from that of adult DRG neurons. Our data show that extensive glycosylation of rat Na(v)1.9 is developmentally regulated and changes a critical property of this channel in native neurons.
Indexed as
Identifiers
11739573PMC6763018W2109914717What 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.