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The Journal of Neuroscience, September 1, 1998, 18(17):6814-6821

Calcium-Evoked Dendritic Exocytosis in Cultured Hippocampal Neurons. Part II: Mediation by Calcium/Calmodulin-Dependent Protein Kinase II

Mirjana Maletic-Savatic, Thillai Koothan, and Roberto Malinow

Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724

Calcium-evoked dendritic exocytosis (CEDE), demonstrated in cultured hippocampal neurons, is a novel mechanism that could play a role in synaptic plasticity. A number of forms of neuronal plasticity are thought to be mediated by calcium/calmodulin-dependent protein kinase II (CaMKII). Here, we investigate the role of CaMKII in CEDE. We find that the developmental time course of CEDE parallels the expression of alpha CaMKII, a dominant subunit of CaMKII. An inhibitor of this enzyme, KN-62, blocks CEDE. Furthermore, 7 d in vitro neurons (which normally do not express alpha CaMKII nor show CEDE) can undergo CEDE when infected with a recombinant virus producing alpha CaMKII. Expression of a constitutively active CaMKII produces dendritic exocytosis in the absence of calcium stimulus, and this exocytosis is blocked by nocodazole, an inhibitor of microtubule polymerization that also blocks CEDE. These results indicate that CEDE is mediated by the activation of CaMKII, consistent with the view that CEDE plays a role in synaptic plasticity.

Key words: FM1-43; exocytosis; dendrites; pyramidal neurons; hippocampal cultures; CaMKII; KN-62; immunocytochemistry; vaccinia virus

Copyright © 1998 Society for Neuroscience  0270-6474/98/18176814-08$05.00/0


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