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defects in the brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway contribute to the deregulated AMPAR trafficking.
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a circuitry in which the upregulation of miR-409-3p and miR-495-3p, belonging to a brain-specific miRNA subcluster implicated in several neurodevelopmental disorders, produced the downregulation of Gria2, is reported.
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GluA2 C-terminus is required for synaptic scaling in CA1 hippocampal pyramidal neurons.
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translocation of surface GluA1, but not GluA2, AMPAR subunits to the synapse requires the amino-terminal domain
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Critically, by altering the two interacting loops of TARP gamma2 and TARP gamma8, the authors could entirely remove all allosteric modulation of GluA2, without affecting formation of AMPA receptor-TARP complexes.
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the GluA2 subunit via its interaction with GAPDH, play a critical role in cortical neurodevelopment.
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The results of this study indicate that disrupting GluA2 phosphorylation leads to increased responsivity to acute stress following cocaine exposure and increased vulnerability to chronic stress.
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Long-term depression proceeds upon stimulation in cerebellar Purkinje cells in mice carrying mutated GluA2 C terminus.
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The data of this study indicated that GluA2-lacking AMPARs are present at D1R-expressing MSN synapses after withdrawal from both contingent and non-contingent cocaine exposure.
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These data suggest that excess mu3A acts independently of the AP-3A complex to reroute AMPAR to recycling endosomes.
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Topological regulation of synaptic AMPA receptor expression by the RNA-binding protein CPEB3 has been demonstrated.
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Results indicate that disrupting GluA2 phosphorylation and increasing GluA2-mediated transmission in the nucleus accumbens leads to increased vulnerability to cocaine relapse.
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Chronic stress-elicited depressive behavior may be due to hypertrophy of basolateral amygdala (BLA) neuronal dendrites and increased of Glur1-Glur2 ratio in BLA neurons.
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found the protein levels of AMPA receptor subunits (GluR1 and GluR2) are upregulated in the amygdala and the 5-HT3 receptor is downregulated in hypothalamic regions of Socially Isolated mice.
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These results provide direct evidence for cortical AMPA receptors to contribute to zymosan-induced visceral and spontaneous pain.
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Animals trained in the trace fear conditioning protocol had GluA2 RNA editing levels were nearly 100% in amygdala and hippocampus.
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These results provide evidence for VPS35's function in promoting spine maturation, which is likely through increasing AMPA receptor targeting to the postsynaptic membrane.
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Bacopa monnieri extract (CDRI-08) upregulates the expression of the GluR2 subunit in the CA3 area of the hippocampus.
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subcellular redistribution of GRIP1 and a change in the binding of GRIP1 to GluA2 during synaptic scaling, was observed.
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Data indicate that the AMPA receptor subunits abundance is hippocampus, GluA2 > GluA1 > GluA3 >> GluA4; cortex, GluA2 > GluA3 >/= GluA1 >> GluA4; and cerebellum, GluA2 > GluA3 >/= GluA1 > GluA4.