Catalytically Dead αCaMKII K42M Mutant Acts as a Dominant Negative in the Control of Synaptic Strength
During long-term potentiation (LTP) of excitatory synapses, Ca2+/calmodulin-dependent protein kinase II (CaMKII) is activated by Ca2+ influx through NMDA receptors that potentiate AMPA receptor currents by insertion of additional GluR1-containing receptors at the synapse and by increasing AMPA chann...
| Main Authors: | , |
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| Format: | Online |
| Language: | English |
| Published: |
Public Library of Science
2015
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| Online Access: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4408036/ |