CONTROL OF CA2+ SIGNALING, FUNCTIONS AND SURVIVAL, BY THE MITOCHONDRIAL NA+/CA2+ EXCHANGER NCLX IN GLIA AND NEURONS

Research output: Chapter in Book/Report/Conference proceedingConference contribution

Abstract

Mitochondria are the energy hub of the cell, but are also central
to Ca2+ signaling. Mitochondrial Ca2+ uptake driven by the
membrane potential enters the mitochondria and is then
pumped out through a mitochondrial Na+/Ca2+ exchanger
NCLX. This mitochondrial ca2+ shuttling couple Ca2+ signaling to metabolic activity and also control the local Ca2+ concentration at ER and plasma membrane domain At the first part
of my talk I will describe the role of the mitochondrial Na+/
Ca2+ exchanger, NCLX in astrocytes We found that NCLX is
responsible for astrocytic mitochondrial Ca2+ extrusion.
Inhibition of NCLX function modulated cytosolic Ca2+ dynamics in astrocytes and had a strong effect on Ca2+ influx
via store-operated entry. In contrast, ER Ca2+ release triggered
only modest mitochondrial Ca2+ transients, indicating that the
functional cross talk between the plasma membrane and mitochondrial domains is particularly strong in astrocytes. Finally
molecularly controlling NCLX shaped Ca2 +−dependent processes in astrocytes such as exocytotic glutamate release,
wound closure, and proliferation. In the final part of my talk I
will describe a novel PKA dependent regulatory site of NCLX
that unregulated NCLX activity following mitochondrial depolarization encountered in neurodegenerative models.
Original languageEnglish GB
Title of host publicationJOURNAL OF NEUROIMMUNE PHARMACOLOGY
PagesS57-S57
Volume11
DOIs
StatePublished - 2016

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