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

Author

Listed:
  • 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
    University of California, San Francisco)

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.

Suggested Citation

  • Salvatore Incontro & Javier Díaz-Alonso & Jillian Iafrati & Marta Vieira & Cedric S. Asensio & Vikaas S. Sohal & Katherine W. Roche & Kevin J. Bender & Roger A. Nicoll, 2018. "The CaMKII/NMDA receptor complex controls hippocampal synaptic transmission by kinase-dependent and independent mechanisms," Nature Communications, Nature, vol. 9(1), pages 1-21, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-04439-7
    DOI: 10.1038/s41467-018-04439-7
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