Erin E. Gray
University of California, Los Angeles
9 Papers
14 Citations
Erin E. Gray is an academic researcher from University of California, Los Angeles. The author has contributed to research in topics: AMPA receptor & Synaptic plasticity. The author has an hindex of 6, co-authored 8 publications.
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Papers
PSD-95 is post-transcriptionally repressed during early neural development by PTBP1 and PTBP2
TL;DR: In this paper, the authors found that postsynaptic density protein 95 (PSD-95) was controlled post-transcriptionally during neural development by two PTB proteins whose sequential downregulation is necessary for synapse maturation.
A Role for Calcium-Permeable AMPA Receptors in Synaptic Plasticity and Learning
Brian J. Wiltgen,Brian J. Wiltgen,Gordon Royle,Erin E. Gray,Andrea Abdipranoto,Nopporn Thangthaeng,Nathan S. Jacobs,Faysal Saab,Susumu Tonegawa,Stephen F. Heinemann,Thomas J. O'Dell,Michael S. Fanselow,Bryce Vissel +12 more
TL;DR: Results suggest that GluR2-lacking AMPARs play a functional and previously unidentified role in learning; they appear to mediate changes in synaptic strength that occur after plasticity has been established by NMDARs.
Fear learning and extinction are linked to neuronal plasticity through Rin1 signaling
TL;DR: It is reported that Rin1−/− mice exhibit profound deficits in both latent inhibition and fear extinction, suggesting a critical role for Rin1 in gating the acquisition and persistence of cue‐dependent fear conditioning, and a correlation between amygdala plasticity and fear learning is demonstrated.
Inhibitory Interactions between Phosphorylation Sites in the C-terminus of α-Amino-3-Hydroxy-5-Methyl-4-Isoxazolepropionic Acid-Type Glutamate Receptor GluA1 Subunits
TL;DR: It is reported that neuronal depolarization in hippocampal slices induces a calcium and protein phosphatase 1/2A-dependent dephosphorylation of GluA1 at Thr-840 and a nearby site at Ser-845, revealing a novel mechanism for regulating AMPAR function at excitatory synapses.
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Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus
TL;DR: It is demonstrated that under certain experimental conditions, Schaffer collateral/commissural fiber stimulation can elicit robust polysynaptic excitatory postsynaptic potentials due to recurrent synaptic inputs onto CA1 pyramidal cells, and activation of presynaptic GABA(B) and adenosine receptors appears to have an important role in activity-dependent depression at recurrent synapses.
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