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• W1952592959 abstract "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 beta 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 kinasebeta 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." @default.
• W1952592959 created "2016-06-24" @default.
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• W1952592959 date "2003-10-29" @default.
• W1952592959 modified "2023-10-01" @default.
• W1952592959 title "Loss of Ca²⁺/Calmodulin Kinase Kinase β Affects the Formation of Some, But Not All, Types of Hippocampus-Dependent Long-Term Memory" @default.
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• W1952592959 doi "https://doi.org/10.1523/jneurosci.23-30-09752.2003" @default.
• W1952592959 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6740881" @default.
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