ArticleMolecular pain2013
Sodium-calcium exchangers in rat trigeminal ganglion neurons.
Article in Molecular pain, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Novel insights into STIM1's role in store-operated calcium entry and its implications for T-cell mediated inflammation in trigeminal neuralgia.Frontiers in molecular neuroscience · 2024Article
- Sodium-Calcium Exchanger-3 Plays Critical Roles in Pain "Wind-up".Neuroscience bulletin · 2023Article
- Functional Coupling between the P2XInternational journal of molecular sciences · 2021Article
- Neuropathic Pain in Multiple Sclerosis and Its Animal Models: Focus on Mechanisms, Knowledge Gaps and Future Directions.Frontiers in neurology · 2021Review
- Article
- Intracellular CaThe journal of physiological sciences : JPS · 2019Article
- Calpain-3-mediated regulation of the Na⁺-Ca²⁺ exchanger isoform 3.Pflugers Archiv : European journal of physiology · 2016Article
- Endogenous opioids contribute to insensitivity to pain in humans and mice lacking sodium channel Nav1.7.Nature communications · 2015Article
- Odontoblasts as sensory receptors: transient receptor potential channels, pannexin-1, and ionotropic ATP receptors mediate intercellular odontoblast-neuron signal transduction.Pflugers Archiv : European journal of physiology · 2015Article
- Functional expression of bradykinin B1 and B2 receptors in neonatal rat trigeminal ganglion neurons.Frontiers in cellular neuroscience · 2015Article
- The properties, distribution and function of Na(+)-Ca(2+) exchanger isoforms in rat cutaneous sensory neurons.The Journal of physiology · 2014Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNoxious stimulation and nerve injury induce an increase in intracellular Ca(2+) concentration ([Ca(2+)]i) via various receptors or ionic channels. While an increase in [Ca(2+)]i excites neurons, [Ca(2+)]i overload elicits cytotoxicity, resulting in cell death. Intracellular Ca(2+) is essential for many signal transduction mechanisms, and its level is precisely regulated by the Ca(2+) extrusion system in the plasma membrane, which includes the Na(+)-Ca(2+) exchanger (NCX). It has been demonstrated that Ca(2+)-ATPase is the primary mechanism for removing [Ca(2+)]i following excitatory activity in trigeminal ganglion (TG) neurons; however, the role of NCXs in this process has yet to be clarified. The goal of this study was to examine the expression/localization of NCXs in TG neurons and to evaluate their functional properties.
resultsNCX isoforms (NCX1, NCX2, and NCX3) were expressed in primary cultured rat TG neurons. All the NCX isoforms were also expressed in A-, peptidergic C-, and non-peptidergic C-neurons, and located not only in the somata, dendrites, axons and perinuclear region, but also in axons innervating the dental pulp. Reverse NCX activity was clearly observed in TG neurons. The inactivation kinetics of voltage-dependent Na(+) channels were prolonged by NCX inhibitors when [Ca(2+)]i in TG neurons was elevated beyond physiological levels.
conclusionsOur results suggest that NCXs in TG neurons play an important role in regulating Ca(2+)-homeostasis and somatosensory information processing by functionally coupling with voltage-dependent Na+ channels.
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