The molecular and cellular biology of enhanced cognition

被引:275
作者
Lee, Yong-Seok
Silva, Alcino J. [1 ]
机构
[1] Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA
关键词
LONG-TERM POTENTIATION; MUTANT MICE LACKING; BIDIRECTIONAL SYNAPTIC PLASTICITY; TISSUE-PLASMINOGEN ACTIVATOR; GROWTH-ASSOCIATED MOLECULE; CYCLIN-DEPENDENT KINASE-5; RUBINSTEIN-TAYBI-SYNDROME; TYPE-1; ADENYLYL-CYCLASE; IMMEDIATE-EARLY GENE; CA3 NMDA RECEPTORS;
D O I
10.1038/nrn2572
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Most molecular and cellular studies of cognitive function have focused on either normal or pathological states, but recent research with transgenic mice has started to address the mechanisms of enhanced cognition. These results point to key synaptic and nuclear signalling events that can be manipulated to facilitate the induction or increase the stability of synaptic plasticity, and therefore enhance the acquisition or retention of information. Here, we review these surprising findings and explore their implications to both mechanisms of learning and memory and to ongoing efforts to develop treatments for cognitive disorders. These findings represent the beginning of a fundamental new approach in the study of enhanced cognition.
引用
收藏
页码:126 / 140
页数:15
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