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The Journal of Neuroscience, July 1, 2002, 22(13):5719-5726
Transgenic Calmodulin-Dependent Protein Kinase II Activation:
Dose-Dependent Effects on Synaptic Plasticity, Learning, and
Memory
Rafael
Bejar1,
Rie
Yasuda2, 4,
Harmen
Krugers3,
Kristin
Hood1, and
Mark
Mayford1, 4
1 Neurosciences Graduate Program, University of
California at San Diego, La Jolla, California 92093, 2 Genomics Institute of the Novartis Research Foundation,
San Diego, California 92121, 3 Swammerdam Institute for
Life Sciences, Section of Neurobiology, University of Amsterdam, 1090GB
The Netherlands, and 4 Department of Cell Biology,
The Scripps Research Institute, La Jolla, California 92037
Genetic disruption of calmodulin-dependent protein kinase II
(CaMKII) function alters hippocampal synaptic plasticity and memory in
mice. We used transgenic mice carrying a tetracycline-regulated, calcium-independent form of CaMKII (CaMKII-Asp286) to investigate the
role of CaMKII activation on synaptic plasticity and behavior. Mice
expressing low levels of a CaMKII-Asp286 transgene have facilitated low-frequency (5 Hz)-induced long-term potentiation (LTP), whereas mice
with high levels of transgene expression have a deficit in this form of
plasticity. Behavioral impairments on fear-conditioned memory and
visible water maze correlate with the level of CaMKII-Asp286 expression. Mice with high levels of CaMKII-Asp286 have reversible, compensatory changes in the expression of genes associated with inhibitory neurotransmission. These results demonstrate that in the
hippocampus, CaMKII activation facilitates the induction of low-frequency LTP, but at high levels of expression, compensatory mechanisms act to inhibit the induction of this form of LTP. The most
severe behavioral impairments are associated with activation of this
compensatory mechanism.
Key words:
memory; CaMKII; mice; transgenic; tetracycline; genetic
compensation; long-term potentiation
Copyright © 2002 Society for Neuroscience 0270-6474/02/22135719-08$05.00/0
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