Aberrant activity of mitochondrial NCLX is linked to impaired synaptic transmission and is associated with mental retardation

Stavsky et al. examined the effects of deleting the mitochondrial sodium/lithium/calcium exchanger, NCLX, on mitochondrial and synaptic calcium homeostasis, synaptic activity, and plasticity in mice. Having identified a human mutation that impairs NCLX activity and is associated with mental retardat...

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Bibliographic Details
Main Authors: Alexandra Stavsky, Ohad Stoler, Marko Kostic, Tomer Katoshevsky, Essam A. Assali, Ivana Savic, Yael Amitai, Holger Prokisch, Steffen Leiz, Cornelia Daumer-Haas, Ilya Fleidervish, Fabiana Perrochi, Daniel Gitler, Israel Sekler
Format: Article
Language:English
Published: Nature Publishing Group 2021-06-01
Series:Communications Biology
Online Access:https://doi.org/10.1038/s42003-021-02114-0
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Summary:Stavsky et al. examined the effects of deleting the mitochondrial sodium/lithium/calcium exchanger, NCLX, on mitochondrial and synaptic calcium homeostasis, synaptic activity, and plasticity in mice. Having identified a human mutation that impairs NCLX activity and is associated with mental retardation, they show that NCLX is crucial for defining synaptic strength and plasticity, which are pivotal elements of learning and memory.
ISSN:2399-3642