NMDAR Ca2+ Boosts synaptic strength
This is a news story, published by Journal of Neuroscience, that relates primarily to NMDA news.
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dendritic spinesJournal of Neuroscience
•Amyloid-β Causes NMDA Receptor Dysfunction and Dendritic Spine Loss through mGluR1 and AKAP150-Anchored Calcineurin Signaling
77% Informative
Neuronal excitatory synapses are located on small dendritic protrusions called spines.
Ca2+ influx through postsynaptic NMDA -type glutamate receptors (NMDARs) initiates signaling pathways that coordinate changes in spine structure and synaptic function.
In Alzheimer's disease, the pathological agent amyloid- (A) may impair learning and memory by biasing NMDAR signaling pathways toward LTD and spine elimination.
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