The CaMKII/NMDA receptor complex controls hippocampal synaptic transmission by kinase-dependent and independent mechanisms

Salvatore Incontro (), Javier Díaz-Alonso, Jillian Iafrati, Marta Vieira, Cedric S. Asensio, Vikaas S. Sohal, Katherine W. Roche, Kevin J. Bender and Roger A. Nicoll ()
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Salvatore Incontro: University of California, San Francisco
Javier Díaz-Alonso: University of California, San Francisco
Jillian Iafrati: University of California, San Francisco
Marta Vieira: National Institutes of Health
Cedric S. Asensio: University of Denver
Vikaas S. Sohal: University of California, San Francisco
Katherine W. Roche: National Institutes of Health
Kevin J. Bender: University of California, San Francisco
Roger A. Nicoll: University of California, San Francisco

Nature Communications, 2018, vol. 9, issue 1, 1-21

Abstract: Abstract CaMKII is one of the most studied synaptic proteins, but many critical issues regarding its role in synaptic function remain unresolved. Using a CRISPR-based system to delete CaMKII and replace it with mutated forms in single neurons, we have rigorously addressed its various synaptic roles. In brief, basal AMPAR and NMDAR synaptic transmission both require CaMKIIα, but not CaMKIIβ, indicating that, even in the adult, synaptic transmission is determined by the ongoing action of CaMKIIα. While AMPAR transmission requires kinase activity, NMDAR transmission does not, implying a scaffolding role for the CaMKII protein instead. LTP is abolished in the absence of CaMKIIα and/or CaMKIIβ and with an autophosphorylation impaired CaMKIIα (T286A). With the exception of NMDAR synaptic currents, all aspects of CaMKIIα signaling examined require binding to the NMDAR, emphasizing the essential role of this receptor as a master synaptic signaling hub.

Date: 2018
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DOI: 10.1038/s41467-018-04439-7

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