Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models
Published 2013 View Full Article
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Title
Suppressing aberrant GluN3A expression rescues synaptic and behavioral impairments in Huntington's disease models
Authors
Keywords
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Journal
NATURE MEDICINE
Volume 19, Issue 8, Pages 1030-1038
Publisher
Springer Nature
Online
2013-07-15
DOI
10.1038/nm.3246
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Note: Only part of the references are listed.- The NMDA receptor subunit GluN3A protects against 3-nitroproprionic-induced striatal lesions via inhibition of calpain activation
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- Phenylbutyrate rescues dendritic spine loss associated with memory deficits in a mouse model of Alzheimer disease
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- Neuroprotection by the NR3A Subunit of the NMDA Receptor
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- Mutant Huntingtin Impairs Vesicle Formation from Recycling Endosomes by Interfering with Rab11 Activity
- (2009) X. Li et al. MOLECULAR AND CELLULAR BIOLOGY
- Balance between synaptic versus extrasynaptic NMDA receptor activity influences inclusions and neurotoxicity of mutant huntingtin
- (2009) Shu-ichi Okamoto et al. NATURE MEDICINE
- Downregulation of NR3A-Containing NMDARs Is Required for Synapse Maturation and Memory Consolidation
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