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The Journal of Neuroscience, October 29, 2003, 23(30):9752-9760

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Cellular/Molecular
Loss of Ca²⁺/Calmodulin Kinase Kinase Affects the Formation of Some, But Not All, Types of Hippocampus-Dependent Long-Term Memory

Marco Peters,¹ Keiko Mizuno,¹ Laurence Ris,^1,2 Marco Angelo,¹ Emile Godaux,² and K. Peter Giese¹

¹Wolfson Institute for Biomedical Research, University College London, London, WC1E 6BT, United Kingdom, and ²Department of Neurosciences, University of Mons-Hainaut, 7000 Mons, Belgium

Long-term memory (LTM) requires activation of the transcription factor cAMP-responsive element binding protein (CREB). Signaling by the Ca²⁺/calmodulin (CaM) kinase cascade has been implicated in CREB activation and memory consolidation processes in the hippocampus. The CaM kinase kinase isoforms belong to the CaM kinase cascade, and we have generated null mutant mice to investigate the role of these kinases in several forms of learning and memory. The null mutants were impaired in spatial training-induced CREB activation and spatial memory formation. Furthermore, the mutants lacked late, but not early, long-term potentiation at the hippocampal CA1 synapse, and they were impaired in LTM, but not short-term memory, for the social transmission of food preferences. We suggest that the CaM kinase kinase isoforms are required for the formation of hippocampal LTM. Surprisingly, however, these kinases were not needed for contextual, trace fear, and passive avoidance LTM. Our results demonstrate that different signaling processes underlie the formation of these types of hippocampal LTM.

Key words: CREB; gene targeting; hippocampus; learning and memory; long-term potentiation; signaling

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Received June 23, 2003; revised September 5, 2003; accepted September 6, 2003.

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