Regulation of synaptic transmission by mitochondrial ion channels

Journal of Bioenergetics and Biomembranes
Elizabeth A Jonas

Abstract

Mitochondria are abundant within neuronal presynaptic terminals, where they provide energy for sustained neurotransmitter secretion. Injection of Bcl-xL protein into squid giant presynaptic terminal potentiates neurotransmitter release, while a naturally occurring, proteolytic fragment of BCL-xL causes rundown of synaptic function. The cleaved form of BCL-xL generates large, multiconductance ion channel activity in synaptic mitochondrial outer membranes. A rapid onset of synaptic rundown can also be produced by depriving the synapse of oxygen, and hypoxia also induces large channel activity in mitochondrial outer membranes. Channel activity induced by cleaved BCL-xL or by hypoxia is attenuated by NADH, an inhibitor of the voltage-dependent anion channel (VDAC) of mitochondrial outer membranes. Finally, the large conductances elicited by hypoxia are prevented by the addition of a protease inhibitor that prevents cleavage of BCL-xL. The opposing activities of BCL-xL and its proteolytic fragment may regulate the release of ATP from mitochondria during synaptic transmission.

Citations

May 16, 2008·The Journal of Neuroscience : the Official Journal of the Society for Neuroscience·Yuliya V MedvedevaYuriy M Usachev
Apr 29, 2009·International Journal of Molecular Sciences·Jolanta SkalskaAdam Szewczyk
May 10, 2006·Proceedings of the National Academy of Sciences of the United States of America·Jianxue LiRichard L Sidman
Jun 21, 2011·International Journal of Developmental Neuroscience : the Official Journal of the International Society for Developmental Neuroscience·Noemí RuedaCarmen Martínez-Cué
Nov 10, 2006·American Journal of Physiology. Cell Physiology·Oliver Kann, Richard Kovács
Apr 3, 2014·Physiological Reviews·Ildiko Szabo, Mario Zoratti

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