The δ2 glutamate receptor gates long-term depression by coordinating interactions between two AMPA receptor phosphorylation sites
Copyright policy )The δ2 glutamate receptor gates long-term depression by coordinating interactions between two AMPA receptor phosphorylation sites
Significance Long-term depression (LTD) commonly affects learning and memory in various brain regions. Although LTD in the cerebellum absolutely requires δ2 glutamate receptors, its underlying mechanisms remain elusive. LTD is caused by endocytosis of AMPA receptors, which is triggered by activity-induced serine phosphorylation of the GluA2 subunit. Our work showed that this serine phosphorylation required prior dephosphorylation of the nearby tyrosine residue. By interaction with a tyrosine phosphatase, δ2 glutamate receptors regulated tyrosine dephosphorylation status of GluA2 to gate inducibility of LTD. These findings will provide better understanding of general mechanisms regulating AMPA receptor endocytosis during synaptic plasticity.
Mice, Knockout, Neuronal Plasticity, Patch-Clamp Techniques, ADP-Ribosylation Factors, Long-Term Synaptic Depression, Models, Neurological, Protein Tyrosine Phosphatase, Non-Receptor Type 4, Mice, Protein Subunits, Purkinje Cells, Receptors, Glutamate, ADP-Ribosylation Factor 6, Cerebellum, Serine, Animals, Guanine Nucleotide Exchange Factors, Protein Interaction Domains and Motifs, Receptors, AMPA, Phosphorylation, Signal Transduction
Mice, Knockout, Neuronal Plasticity, Patch-Clamp Techniques, ADP-Ribosylation Factors, Long-Term Synaptic Depression, Models, Neurological, Protein Tyrosine Phosphatase, Non-Receptor Type 4, Mice, Protein Subunits, Purkinje Cells, Receptors, Glutamate, ADP-Ribosylation Factor 6, Cerebellum, Serine, Animals, Guanine Nucleotide Exchange Factors, Protein Interaction Domains and Motifs, Receptors, AMPA, Phosphorylation, Signal Transduction
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