Sodium-Calcium Exchangers in Rat Trigeminal Ganglion Neurons

• Published in: Molecular pain 2013-04, Vol.9 (1), p.22-22
• Main Authors: Kuroda, Hidetaka, Sobhan, Ubaidus, Sato, Masaki, Tsumura, Maki, Ichinohe, Tatsuya, Tazaki, Masakazu, Shibukawa, Yoshiyuki
• Format: Article
• Language: English
• Subjects: Adenosine triphosphatase; Animals; Axons - drug effects; Axons - metabolism; Calcium; Calcium - pharmacology; Cell death; Cells, Cultured; Cellular signal transduction; Colleges & universities; Cryoultramicrotomy; Dental Pulp - cytology; Dental Pulp - drug effects; Dental Pulp - innervation; Experiments; Female; Ganglion; Ion Channel Gating - drug effects; Kinetics; Male; Neurons; Neurons - cytology; Neurons - drug effects; Neurons - metabolism; Potassium - pharmacology; Protein Isoforms - genetics; Protein Isoforms - metabolism; Proteins; Rats; Rats, Wistar; Real-Time Polymerase Chain Reaction; RNA, Messenger - genetics; RNA, Messenger - metabolism; Rodents; Signal transduction; Sodium; Sodium-Calcium Exchanger - genetics; Sodium-Calcium Exchanger - metabolism; Software; Trigeminal Ganglion - cytology; Trigeminal Ganglion - drug effects; Trigeminal Ganglion - metabolism; Voltage-Gated Sodium Channels - metabolism
• ISSN: 1744-8069; 1744-8069
• DOI: 10.1186/1744-8069-9-22

Background Noxious stimulation and nerve injury induce an increase in intracellular Ca2+ concentration ([Ca2+]i) via various receptors or ionic channels. While an increase in [Ca2+]i excites neurons, [Ca2+]i overload elicits cytotoxicity, resulting in cell death. Intracellular Ca2+ is essential for many signal transduction mechanisms, and its level is precisely regulated by the Ca2+ extrusion system in the plasma membrane, which includes the Na+-Ca2+ exchanger (NCX). It has been demonstrated that Ca2+-ATPase is the primary mechanism for removing [Ca2+]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. Results NCX 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 [Ca2+]i in TG neurons was elevated beyond physiological levels. Conclusions Our results suggest that NCXs in TG neurons play an important role in regulating Ca2+-homeostasis and somatosensory information processing by functionally coupling with voltage-dependent Na+ channels.