Na+/Ca2+ exchange and Ca2+ homeostasis in axon terminals of mammalian central neurons

Suk Ho Lee, Myoung Hwan Kim, Ju Young Lee, Hun Lee Sang, Doyun Lee, Han Park Kyeong, Won Kyung Ho

Research output: Chapter in Book/Report/Conference proceedingConference contributionpeer-review

9 Scopus citations

Abstract

We investigated Ca2+ clearance mechanisms (CCMs) at the axon terminals of mammalian central neurons: neurohypophysial (NHP) axon terminals and calyces of Held. Ca2+ transients were evoked by applying a short depolarization pulse via a patch pipette containing Ca2+ indicator dye. Quantitative analysis of the Ca2+ decay phases revealed that Na+/Ca2+ exchange (Na/CaX) is a major CCM at both axon terminals. In contrast, no Na/CaX activity was found in the somata of NHP axon terminals (supraoptic magnocellular neurons), indicating that the distribution of Na+/Ca2+ exchangers is polarized. Intracellular dialysis of axon terminals with a K+-free pipette solution attenuated the Na/CaX activities by 90% in the NHP axon terminals and by 60% at the calyx of Held, indicating that K+-dependent Na+/Ca2+ exchangers are involved. Studying the effects of specific inhibitors of smooth endoplasmic reticulum Ca2+-ATPase (SERCA) and plasma membrane Ca 2+-ATPase (PMCA) on the Ca2+ decay rate revealed thatPMCAcontributed 23% of total Ca2+ clearance, but that SERCA made no contribution at the calyx of Held. The contribution of mitochondria was negligible for small Ca2+ transients, but became apparent at peak Ca2+ levels higher than 2.5 μM. When mitochondrial function was inhibited, the dependence of CCMs on [Ca2+]i at the calyx of Held showed saturation kinetics with K1/2 = 1.7 μM, suggesting that the Na/CaX activity is saturated at high [Ca2+]i. The presynaptic Na+/Ca2+ exchanger activity, which competes for cytosolic Ca2+ with mitochondria, may contribute to nonplastic synaptic transmission at these axon terminals.

Original languageEnglish
Title of host publicationSodium-Calcium Exchange and the Plasma Membrane Ca2+ATPase in Ce;; Funcyion
Subtitle of host publicationFifth International Conference
PublisherBlackwell Publishing Inc.
Pages396-412
Number of pages17
ISBN (Print)1573316490, 9781573316491
DOIs
StatePublished - Mar 2007

Publication series

NameAnnals of the New York Academy of Sciences
Volume1099
ISSN (Print)0077-8923
ISSN (Electronic)1749-6632

Keywords

  • Calyx of Held
  • Mitochondria
  • NCKX
  • NCX
  • Neurohypophysial axon terminals
  • Supraoptic magnocellular neuron

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