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 Ca2+-ATPase (PMCA) on the Ca2+ decay rate revealed that PMCA contributed 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 microM. When mitochondrial function was inhibited, the dependence of CCMs on [Ca2+]i at the calyx of Held showed saturation kinetics with K(1/2) = 1.7 microM, 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.
journal_name
Ann N Y Acad Scijournal_title
Annals of the New York Academy of Sciencesauthors
Lee SH,Kim MH,Lee JY,Lee SH,Lee D,Park KH,Ho WKdoi
10.1196/annals.1387.011subject
Has Abstractpub_date
2007-03-01 00:00:00pages
396-412eissn
0077-8923issn
1749-6632pii
1099/1/396journal_volume
1099pub_type
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