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Open AccessJournal ArticleDOI

Subunit Composition of Synaptic AMPA Receptors Revealed by a Single-Cell Genetic Approach

TLDR
A functional quantification of the subunit composition of AMPARs in the CNS is provided and novel roles for AMPAR subunits in receptor trafficking are suggested and suggested.
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This article is published in Neuron.The article was published on 2009-04-30 and is currently open access. It has received 605 citations till now. The article focuses on the topics: Silent synapse & Long-term depression.

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Journal ArticleDOI

miR‐181a negatively modulates synaptic plasticity in hippocampal cultures and its inhibition rescues memory deficits in a mouse model of Alzheimer’s disease

TL;DR: The results indicate that miR‐181a is a major negative regulator of the cellular events that underlie synaptic plasticity and memory through AMPA receptors, and importantly, Aβ disrupts this process by suppressing translin and leads to synaptic dysfunction and memory impairments in AD.
Journal ArticleDOI

Coupled Activity-Dependent Trafficking of Synaptic SK2 Channels and AMPA Receptors

TL;DR: The ∼2 h window after the induction of LTP during which synaptic SK2 activity is absent may be important for consolidating the later phases of LTT, and the LTP-dependent endocytosis of SK2 is coupled to L TP-dependent AMPA exocytotic.
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Exposure of neurons to excitotoxic levels of glutamate induces cleavage of the RNA editing enzyme, adenosine deaminase acting on RNA 2, and loss of GLUR2 editing.

TL;DR: It is demonstrated that cleaved ADAR2 leads to a decrease or loss of GluR2 editing, which will further result in high Ca2+ influx and excitotoxic neuronal death.
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Loss of α1,6-Fucosyltransferase Decreases Hippocampal Long Term Potentiation IMPLICATIONS FOR CORE FUCOSYLATION IN THE REGULATION OF AMPA RECEPTOR HETEROMERIZATION AND CELLULAR SIGNALING

TL;DR: Loss of core fucosylation on AMPARs enhanced their heteromerization, which increase sensitivity for postsynaptic depolarization and persistently activate N-methyl-d-aspartate receptors as well as Ca2+ influx and CaMKII and then impair LTP.
References
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Journal Article

The glutamate receptor ion channels

TL;DR: The cloning of cDNAs encoding glutamate receptor subunits, which occurred mainly between 1989 and 1992, stimulated the development of ionotropic glutamate receptors in the brain.
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Cloned Glutamate Receptors

TL;DR: The application of molecular cloning technology to the study of the glutamate receptor system has led to an explosion of knowledge about the structure, expression, and function of this most important fast excitatory transmitter system in the mammalian brain.
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AMPA Receptor Trafficking and Synaptic Plasticity

TL;DR: The growing literature that supports a critical role for AMPA receptors trafficking in LTP and LTD is reviewed, focusing on the roles proposed for specific AMPA receptor subunits and their interacting proteins.
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Driving AMPA Receptors into Synapses by LTP and CaMKII: Requirement for GluR1 and PDZ Domain Interaction

TL;DR: Results show that LTP and CaMKII activity drive AMPA-Rs to synapses by a mechanism that requires the association between GluR1 and a PDZ domain protein.
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RNA editing in brain controls a determinant of ion flow in glutamate-gated channels.

TL;DR: It is shown that the genomic DNA sequences encoding the particular channel segment of all subunits harbor a glutamine codon (CAG), even though an arginine codon is found in mRNAs of three subunits.
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