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Synaptic Tagging and Capture pp 3–12Cite as

Differential Role of CaMK in Synaptic Tagging and Capture

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Abstract

Long-term potentiation (LTP) of synaptic connectivity is theorized to be a physiological correlate of memory formation. Changes in synaptic strength, as well as their maintenance, depend on a network of chemical interactions that occur both locally at the synapse and across the dendrites, axons, and nucleus of the neuron. The Calmodulin Kinase (CaMK) family can be divided into CaMKI/IV and CaMKII subfamilies among others, all with central roles in synaptic plasticity. The question that we address in this chapter is whether the necessary roles of particular CaM Kinases in LTP are restricted to the synthesis of plasticity-related products or to the local phosphorylation of synaptic proteins. We use analytically powerful three-pathway protocols and kinase-specific drugs to dissociate the distinct roles of the CaMK pathways in LTP.

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Authors and Affiliations

  1. Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Room 46-5289, 43 Vassar Street, Cambridge, MA, 02139, USA

    Roger L. Redondo

  2. Center for Cognitive and Neural Systems, The University of Edinburgh, Edinburgh, UK

    Richard G. M. Morris

Authors
  1. Roger L. Redondo
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  2. Richard G. M. Morris
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Corresponding author

Correspondence to Roger L. Redondo .

Editor information

Editors and Affiliations

  1. Yong Loo Lin School of Medicine Department of Physiology, National University of Singapore, Singapore, Singapore

    Sreedharan Sajikumar

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Redondo, R.L., Morris, R.G.M. (2015). Differential Role of CaMK in Synaptic Tagging and Capture. In: Sajikumar, S. (eds) Synaptic Tagging and Capture. Springer, New York, NY. https://doi.org/10.1007/978-1-4939-1761-7_1

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