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

摘要: Cortical plasticity seems to be critical for the establishment of permanent memory traces1,2,3. Little is known, however, about molecular and cellular processes that support consolidation memories in cortical networks4,5. Here we show mice heterozygous a null mutation α-calcium-calmodulin kinase II (α-CaMKII+/-) normal learning 1–3 days after training two hippocampus-dependent tasks. However, their severely impaired at longer retention delays (10–50 days). Consistent with this, found α-CaMKII+/- have cortical, but not hippocampal, long-term potentiation. Our results represent first step unveiling mechanisms underlying memories, they indicate α-CaMKII may modulate synaptic events required traces networks.