α-CaMKII-dependent plasticity in the cortex is required for permanent memory

Paul W. Frankland, Cara O'Brien, Masuo Ohno, Alfredo Kirkwood, Alcino J. Silva

Research output: Contribution to journalArticle

Abstract

Cortical plasticity seems to be critical for the establishment of permanent memory traces. Little is known, however, about the molecular and cellular processes that support consolidation of memories in cortical networks. Here we show that mice heterozygous for a null mutation of α-calcium-calmodulin kinase II (α-CaMKII+/-) show normal learning and memory 1-3 days after training in two hippocampus-dependent tasks. However, their memory is severely impaired at longer retention delays (10-50 days). Consistent with this, we found that α-CaMKII+/- mice have impaired cortical, but not hippocampal, long-term potentiation. Our results represent a first step in unveiling the molecular and cellular mechanisms underlying the establishment of permanent memories, and they indicate that α-CaMKII may modulate the synaptic events required for the consolidation of memory traces in cortical networks.

Original languageEnglish (US)
Pages (from-to)309-313
Number of pages5
JournalNature
Volume411
Issue number6835
DOIs
StatePublished - May 17 2001

ASJC Scopus subject areas

  • General

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    Frankland, P. W., O'Brien, C., Ohno, M., Kirkwood, A., & Silva, A. J. (2001). α-CaMKII-dependent plasticity in the cortex is required for permanent memory. Nature, 411(6835), 309-313. https://doi.org/10.1038/35077089