ArticleJournal of neurophysiology2014
NaV1.5 sodium channel window currents contribute to spontaneous firing in olfactory sensory neurons.
Article in Journal of neurophysiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed.
- Late IMedicinal research reviews · 2026Review
- Immature olfactory sensory neurons are intrinsically excitable and show maturation-dependent changes in voltage-gated NaPflugers Archiv : European journal of physiology · 2026Article
- Distribution of Voltage-Gated Sodium Channels and Scaffolding Proteins on Vestibular Calyx Ending Delineates the Axon Initial Segment.The Journal of comparative neurology · 2026Article
- Nerve Excitability in Asymptomatic Carriers and Amyotrophic Lateral Sclerosis Patients With C9orf72.Annals of clinical and translational neurology · 2025Article
- Perceptual constancy for an odor is acquired through changes in primary sensory neurons.Science advances · 2024Article
- Safinamide, an inhibitor of monoamine oxidase, modulates the magnitude, gating, and hysteresis of sodium ion current.BMC pharmacology & toxicology · 2024Article
- Review
- The Evidence for Effective Inhibition ofInternational journal of molecular sciences · 2022Article
- Growth Differentiation Factor-15 Produces Analgesia by Inhibiting Tetrodotoxin-Resistant Nav1.8 Sodium Channel Activity in Rat Primary Sensory Neurons.Neuroscience bulletin · 2021Article
- Article
- A Comparison of the Primary Sensory Neurons Used in Olfaction and Vision.Frontiers in cellular neuroscience · 2020Review
- Molecular expression of multiple Nav1.5 splice variants in the frontal lobe of the human brain.International journal of molecular medicine · 2018Article
- Regional and Developmental Differences in NaFrontiers in cellular neuroscience · 2018Article
- Distribution and function of voltage-gated sodium channels in the nervous system.Channels (Austin, Tex.) · 2017Review
- Article
- Multiple Nav1.5 isoforms are functionally expressed in the brain and present distinct expression patterns compared with cardiac Nav1.5.Molecular medicine reports · 2017Article
- 5HTR3A-driven GFP labels immature olfactory sensory neurons.The Journal of comparative neurology · 2017Article
- Nonlinear effects of hyperpolarizing shifts in activation of mutant NaJournal of neurophysiology · 2017Article
- Organization and Plasticity of Sodium Channel Expression in the Mouse Olfactory and Vomeronasal Epithelia.Frontiers in neuroanatomy · 2017Article
- Spontaneously active NaV1.5 sodium channels may underlie odor sensitivity.Journal of neurophysiology · 2016Article
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Authors and funding
7 authors.
Funding
Abstract
Olfactory sensory neurons (OSNs) fire spontaneously as well as in response to odor; both forms of firing are physiologically important. We studied voltage-gated Na(+) channels in OSNs to assess their role in spontaneous activity. Whole cell patch-clamp recordings from OSNs demonstrated both tetrodotoxin-sensitive and tetrodotoxin-resistant components of Na(+) current. RT-PCR showed mRNAs for five of the nine different Na(+) channel α-subunits in olfactory tissue; only one was tetrodotoxin resistant, the so-called cardiac subtype NaV1.5. Immunohistochemical analysis indicated that NaV1.5 is present in the apical knob of OSN dendrites but not in the axon. The NaV1.5 channels in OSNs exhibited two important features: 1) a half-inactivation potential near -100 mV, well below the resting potential, and 2) a window current centered near the resting potential. The negative half-inactivation potential renders most NaV1.5 channels in OSNs inactivated at the resting potential, while the window current indicates that the minor fraction of noninactivated NaV1.5 channels have a small probability of opening spontaneously at the resting potential. When the tetrodotoxin-sensitive Na(+) channels were blocked by nanomolar tetrodotoxin at the resting potential, spontaneous firing was suppressed as expected. Furthermore, selectively blocking NaV1.5 channels with Zn(2+) in the absence of tetrodotoxin also suppressed spontaneous firing, indicating that NaV1.5 channels are required for spontaneous activity despite resting inactivation. We propose that window currents produced by noninactivated NaV1.5 channels are one source of the generator potentials that trigger spontaneous firing, while the upstroke and propagation of action potentials in OSNs are borne by the tetrodotoxin-sensitive Na(+) channel subtypes.
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