Opposite regulation of inhibitory synaptic plasticity by α and β subunits of Ca 2+ /calmodulin‐dependent protein kinase II
Author:
Affiliation:
1. Department of BiophysicsGraduate School of ScienceKyoto University Sakyo‐ku Kyoto 606‐8502 Japan
2. Graduate School of Brain ScienceDoshisha University Kizugawa‐shi Kyoto 619‐0025 Japan
Funder
Ministry of Education, Culture, Sports, Science and Technology
Publisher
Wiley
Subject
Physiology
Link
https://onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2014.280230
Reference52 articles.
1. NMDA Receptor Subunit Composition Controls Synaptic Plasticity by Regulating Binding to CaMKII
2. Interaction with the NMDA receptor locks CaMKII in an active conformation
3. Transition from Reversible to Persistent Binding of CaMKII to Postsynaptic Sites and NR2B
4. Developmental expression of the CaM kinase II isoforms: ubiquitous γ- and δ-CaM kinase II are the early isoforms and most abundant in the developing nervous system
5. CaMKII Plays a Nonenzymatic Role in Hippocampal Synaptic Plasticity and Learning by Targeting CaMKII to Synapses
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