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Non-ionotropic signaling through the NMDA receptor GluN2B carboxy terminal domain drives morphological plasticity of dendritic spines and reverses fragile X phenotypes in mouse hippocampus

2024-12-16

Abstract excerpt

<h4>ABSTRACT</h4> It is well known that activation of NMDA receptors can trigger long-term synaptic depression (LTD) and that a morphological correlate of this functional plasticity is spine retraction and elimination. Recent studies have led to the surprising conclusion that NMDA-induced spine shrinkage proceeds independently of ion flux and requires the initiation of de novo protein synthesis, highlighting an...

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Literature Corpus work
e0837d18-1d94-5d87-bcc2-fd0cf4f410c8
DOI
10.1101/2024.12.15.628559
Open publication

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Non-ionotropic signaling through the NMDA receptor GluN2B carboxy terminal domain drives morphological plasticity of dendritic spines and reverses fragile X phenotypes in mouse hippocampusDOI 10.1101/2024.12.15.628559
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