title: Sodium-calcium exchangers in rat trigeminal ganglion neurons.
abstract: BACKGROUND
  Noxious 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.
  
  
  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 [Ca(2+)]i in TG neurons was elevated beyond physiological levels.
  
  
  CONCLUSIONS
  Our 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.
authors.affiliation: Oral Health Science Center hrc8, Tokyo Dental College, Tokyo 261-8502, Japan.
authors.forename: Hidetaka
authors.initials: H
authors.lastname: Kuroda
authors.forename: Ubaidus
authors.initials: U
authors.lastname: Sobhan
authors.forename: Masaki
authors.initials: M
authors.lastname: Sato
authors.forename: Maki
authors.initials: M
authors.lastname: Tsumura
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Ichinohe
authors.forename: Masakazu
authors.initials: M
authors.lastname: Tazaki
authors.forename: Yoshiyuki
authors.initials: Y
authors.lastname: Shibukawa
mesh_terms: D000818:Animals; D001369:Axons / Q000187:drug effects / Q000378:metabolism; D002118:Calcium / Q000494:pharmacology; D002478:Cells, Cultured; D016616:Cryoultramicrotomy; D003782:Dental Pulp / Q000166:cytology / Q000187:drug effects / Q000294:innervation; D005260:Female; D015640:Ion Channel Gating / Q000187:drug effects; D007700:Kinetics; D008297:Male; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D011188:Potassium / Q000494:pharmacology; D020033:Protein Isoforms / Q000235:genetics / Q000378:metabolism; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D060888:Real-Time Polymerase Chain Reaction; D019831:Sodium-Calcium Exchanger / Q000235:genetics / Q000378:metabolism*; D012668:Trigeminal Ganglion / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D061566:Voltage-Gated Sodium Channels / Q000378:metabolism
chemical_list: D020033:Protein Isoforms; D012333:RNA, Messenger; D019831:Sodium-Calcium Exchanger; D061566:Voltage-Gated Sodium Channels; D011188:Potassium; D002118:Calcium