Molecular and cellular mechanisms of cognitive function: Implications for psychiatric disorders

被引:19
|
作者
Silva, AJ
Elgersma, Y
Costa, RM
机构
[1] Univ Calif Los Angeles, Dept Neurobiol, Los Angeles, CA 90095 USA
[2] Univ Calif Los Angeles, Dept Psychiat, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Dept Psychol, Los Angeles, CA 90095 USA
[4] Univ Calif Los Angeles, Brain Res Inst, Los Angeles, CA 90095 USA
关键词
synaptic plasticity; CaMKII; CREB; NF1; schizophrenia; depression;
D O I
10.1016/S0006-3223(99)00294-2
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Recent studies on the molecular non cellular basis of learning and memory have brought us closer than ever to understanding the mechanisms of synaptic plasticity and their relevance to memory formulation. Genetic approaches have played a central role in these new findings because the same mutant mice can be studied with molecular, cellular, circuit, and behavioral tools. Therefore, the results can be used to construct models that cut across levels of analytical complexity, forging connections from the biochemistry of the modified protein to the behavior of the mutant mice. These findings are not only improving our understanding of learning and memory, they are also enriching our understanding of cognitive disorders, such as neurofibromatosis type I. Mechanisms underlying longterm changes in synaptic function are likely to be at the heart of many cognitive and emotional processes in humans. Therefore, molecular and cellular insights into learning and memory undoubtedly will have a profound impact on the understanding and treatment of psychiatric disorders. Biol Psychiatry 2000;47:200-209 (C) 2000 Society of Biological Psychiatry.
引用
收藏
页码:200 / 209
页数:10
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