Disrupted expression of mitochondrial NCLX sensitizes neuroglial networks to excitotoxic stimuli and renders synaptic activity toxic
Anna M. Hagenston(Heidelberg University), Hilmar Bading(Heidelberg University), Jing Yan(University of Massachusetts Chan Medical School), Yan-Wei Tan(Center for Neurosciences), Israel Sekler(Ben-Gurion University of the Negev), Carlos Bas‐Orth(Heidelberg University)
Cited by 19
Related Papers
Synaptic versus extrasynaptic NMDA receptor signalling: implications for neurodegenerative disorders
|Nature reviews. Neuroscience|2010|1.6k
NCLX is an essential component of mitochondrial Na <sup>+</sup> /Ca <sup>2+</sup> exchange
|Proceedings of the National Academy of Sciences|2009|776
Zinc in the physiology and pathology of the CNS
|Nature reviews. Neuroscience|2009|759
A zinc-sensing receptor triggers the release of intracellular Ca <sup>2+</sup> and regulates ion transport
|Proceedings of the National Academy of Sciences|2001|257
Synaptically Released Zinc Triggers Metabotropic Signaling via a Zinc-Sensing Receptor in the Hippocampus
|Journal of Neuroscience|2009|229