Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses

Hojjati, M.R. and Van Woerden, G.M. and Tyler, W.J. and Giese, K.P. and Silva, A.J. and Pozzo-Miller, L. and Elgersma, Y. (2007) Kinase activity is not required for αCaMKII-dependent presynaptic plasticity at CA3-CA1 synapses. Nature Neuroscience, 10 (9). pp. 1125-1127.

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Abstract

Using targeted mouse mutants and pharmacologic inhibition of αCaMKII, we demonstrate that the αCaMKII protein, but not its activation, autophosphorylation or its ability to phosphorylate synapsin I, is required for normal short-term presynaptic plasticity. Furthermore, αCaMKII regulates the number of docked vesicles independent of its ability to be activated. These results indicate that αCaMKII has a nonenzymatic role in short-term presynaptic plasticity at hippocampal CA3-CA1 synapses. © 2007 Nature Publishing Group.

Item Type: Article
Additional Information: cited By
Uncontrolled Keywords: protein kinase (calcium,calmodulin) II, article; enzyme activity; enzyme inhibition; enzyme phosphorylation; enzyme regulation; hippocampus; nerve cell plasticity; nonhuman; priority journal, Analysis of Variance; Animals; Calcium-Calmodulin-Dependent Protein Kinase Kinase; Electric Stimulation; Enzyme Activation; Excitatory Postsynaptic Potentials; Hippocampus; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microscopy, Electron, Transmission; Mutagenesis; Neuronal Plasticity; Neurons; Patch-Clamp Techniques; Phosphorylation; Presynaptic Terminals; Synapses; Synapsins; Synaptic Transmission; Synaptic Vesicles
Subjects: WL Nervous system
Divisions: Faculty of Medicine > Basic Sciences Academic Groups > Department of Physiology
Depositing User: zahra bagheri .
Date Deposited: 21 Aug 2017 06:06
Last Modified: 21 Aug 2017 06:06
URI: http://eprints.skums.ac.ir/id/eprint/3400

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