DEFICIENT HIPPOCAMPAL LONG-TERM POTENTIATION IN ALPHA-CALCIUM-CALMODULIN KINASE-II MUTANT MICE
DEFICIENT HIPPOCAMPAL LONG-TERM POTENTIATION IN ALPHA-CALCIUM-CALMODULIN KINASE-II MUTANT MICE
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DOI：
10.1126/science.1378648
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发表时间：
1992-07-10
期刊：
影响因子：
56.9
通讯作者：
WANG, YY
中科院分区：
文献类型：
--
作者：
SILVA, AJ;STEVENS, CF;WANG, YY
作为在记忆机制研究中使用基因改变小鼠的计划的第一步，产生了不表达α-钙-钙调蛋白依赖性激酶II（α-CaMKII）的突变小鼠。α-CaMKII在海马和新皮层的突触后密度中高度富集，并且可能参与长时程增强（LTP）的调节。这些突变小鼠表现出大多数正常的行为，并没有明显的神经解剖缺陷。全细胞记录显示，突触后机制，包括N-甲基-D-天冬氨酸（NMDA）受体功能，是完整的。尽管有正常的突触后机制，这些小鼠缺乏产生LTP的能力，因此是研究LTP和学习过程之间关系的合适模型。
As a first step in a program to use genetically altered mice in the study of memory mechanisms, mutant mice were produced that do not express the alpha-calcium-calmodulin-dependent kinase II (alpha-CaMKII). The alpha-CaMKII is highly enriched in postsynaptic densities of hippocampus and neocortex and may be involved in the regulation of long-term potentiation (LTP). Such mutant mice exhibited mostly normal behaviors and presented no obvious neuroanatomical defects. Whole cell recordings reveal that postsynaptic mechanisms, including N-methyl-D-aspartate (NMDA) receptor function, are intact. Despite normal postsynaptic mechanisms, these mice are deficient in their ability to produce LTP and are therefore a suitable model for studying the relation between LTP and learning processes.