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Science 10 July 1992:
Vol. 257. no. 5067, pp. 201 - 206
DOI: 10.1126/science.1378648

Articles

Science, Vol 257, Issue 5067, 201-206
Copyright © 1992 by American Association for the Advancement of Science


articles

Deficient hippocampal long-term potentiation in alpha-calcium-calmodulin kinase II mutant mice

AJ Silva, CF Stevens, S Tonegawa, and Y Wang

Howard Hughes Medical Institute, Center for Cancer Research, Cambridge, MA.

As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII). The alpha-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.


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Impaired Synaptic Plasticity and cAMP Response Element-Binding Protein Activation in Ca2+/Calmodulin-Dependent Protein Kinase Type IV/Gr-Deficient Mice.
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Three-dimensional Reconstructions of Calcium/Calmodulin-dependent (CaM) Kinase IIalpha and Truncated CaM Kinase IIalpha Reveal a Unique Organization for Its Structural Core and Functional Domains.
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Dissection of behavior and psychiatric disorders using the mouse as a model.
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Hum. Mol. Genet. 9, 953-965
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Driving AMPA Receptors into Synapses by LTP and CaMKII: Requirement for GluR1 and PDZ Domain Interaction.
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Distinct Roles for Ionotropic and Metabotropic Glutamate Receptors in the Maturation of Excitatory Synapses.
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The genetic basis of cognition.
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Tetanic Stimulation Leads to Increased Accumulation of Ca2+/Calmodulin-Dependent Protein Kinase II via Dendritic Protein Synthesis in Hippocampal Neurons.
Y. Ouyang, A. Rosenstein, G. Kreiman, E. M. Schuman, and M. B. Kennedy (1999)
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Toward a Molecular Explanation for Long-Term Potentiation.
J. D. Sweatt (1999)
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Nitric Oxide Acts as a Postsynaptic Signaling Molecule in Calcium/Calmodulin-Induced Synaptic Potentiation in Hippocampal CA1 Pyramidal Neurons.
G. Y. Ko and P. T. Kelly (1999)
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Dynamic Control of CaMKII Translocation and Localization in Hippocampal Neurons by NMDA Receptor Stimulation.
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