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The Function of CaM Kinase II in Synaptic Plasticity and Spine Formation

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Handbook of Neurochemistry and Molecular Neurobiology

Abstract

Recent advances in molecular genetics provide strong evidence for a relationship between hippocampal long-term potentiation (LTP) and hippocampus-dependent memory. Genetic deletion of a crucial Ca2+/calmodulin-dependent protein kinase II (CaMKII) subunit or inhibition of its autophosphorylation blocks LTP induction and causes severe hippocampus-dependent memory deficits. Synaptic activity-dependent phosphorylation and trafficking of the GluR1 subunit through CaMKII activation account for hippocampal LTP. Moreover, CaMKII activation mediates rapid morphological changes in dendritic spines at excitatory synapses during LTP induction. In addition to the critical role played by CaMKII in synaptic plasticity in various brain regions, various psychotic disorders, including mental retardation, schizophrenia, and depression, alter CaMKII activity in specific brain regions correlated with changes in spine morphology. In this chapter, we focus on CaMKII-dependent mechanisms of memory formation and spine formation in the brain.

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Abbreviations

AMPA:

(S)-α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate

CaM:

calmodulin

CaMKII:

Ca2+/calmodulin-dependent protein kinase II

GluR:

glutamate receptor

LTD:

long-term depression

LTP:

long-term potentiation

NMDA:

N-methyl-D-aspartate

PKC:

protein kinase C

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Fukunaga, K., Shioda, N., Miyamoto, E. (2009). The Function of CaM Kinase II in Synaptic Plasticity and Spine Formation. In: Lajtha, A., Mikoshiba, K. (eds) Handbook of Neurochemistry and Molecular Neurobiology. Springer, Boston, MA. https://doi.org/10.1007/978-0-387-30370-3_9

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