Abnormal long-lasting synaptic plasticity and cognition in mice lacking the mental retardation gene Pak3
Abnormal long-lasting synaptic plasticity and cognition in mice lacking the mental retardation gene Pak3
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DOI：
10.1523/jneurosci.0028-05.2005
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发表时间：
2005-07-13
影响因子：
5.3
通讯作者：
Jia, ZP
中科院分区：
文献类型：
--
作者：
Meng, JS;Meng, YH;Jia, ZP
Pak3 基因突变会导致非综合征性智力低下，其特征是选择性认知缺陷。然而，其根本机制尚待阐明。我们在此报道，p21激活激酶3（PAK3）表达缺陷的基因敲除小鼠表现出突触可塑性的显着异常，特别是海马后期长时程增强，以及学习和记忆缺陷。敲除小鼠中转录因子 cAMP 反应元件结合蛋白活性形式的显着减少暗示了 PAK3 和 Rho 信号传导调节突触功能和认知的新信号传导机制。
Mutations in the Pak3 gene lead to nonsyndromic mental retardation characterized by selective deficits in cognition. However, the underlying mechanisms are yet to be elucidated. We report here that the knock-out mice deficient in the expression of p21-activated kinase 3 (PAK3) exhibit significant abnormalities in synaptic plasticity, specifically hippocampal late-phase long-term potentiation, and deficiencies in learning and memory. A dramatic reduction in the active form of transcription factor cAMP-responsive element-binding protein in the knock-out mice implicates a novel signaling mechanism by which PAK3 and Rho signaling regulate synaptic function and cognition.