A single brief burst induces GluR1-dependent associative short-term potentiation: a potential mechanism for short-term memory.

A single brief burst induces GluR1-dependent associative short-term potentiation: a potential mechanism for short-term memory.
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DOI:
10.1162/jocn.2009.21375
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发表时间:
2010-11
影响因子:
3.2
通讯作者:
Lisman J
Lisman J
中科院分区:
医学3区
文献类型:
--
作者:
Erickson MA;Maramara LA;Lisman J

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最近的工作[Sanderson,D.,Good,M.A.,Skelton,K.,Sprengel,R.,Seeburg,P.H.,Nicholas,J.等人。GluA1 AMPA受体亚单位基因敲除小鼠长期和短期空间记忆增强:双过程记忆模型的证据。学习和记忆,在新闻]表明,短期记忆(STM)选择性地减少在GluR1基因敲除的小鼠。这增加了一种可能性,即依赖于GluR1的突触修饰可能是STM的基础。对突触可塑性的研究表明,太弱而不能诱导长时程增强的刺激会诱发短时程增强(STP),这是一种鲜有人关注的现象。在这里,我们研究了STP的几个属性,并测试了STP对GluR1的依赖性。使用测试路径和条件路径检查了诱导STP的最低要求。测试路径中几个间隔很近的刺激,形成一个短暂的爆发,足以诱导STP。因此,STP很可能是由体内发生的类似爆发引起的。STP诱导在本质上是联想的,并且依赖于NMDAR。STP的衰减有两个分量,一个是快分量(1.6±0.26分钟),一个是慢分量(19±6.6分钟)。为了测试GluR1在STP中的作用,我们在GluR1基因敲除的小鼠上进行了实验。我们发现STP大大降低了。这些结果与D.Sanderson等人的行为工作结合在一起。[Sanderson,D.,Good,M.A.,Skelton,K.,Sprengel,R.,Seeburg,P.H.,Nicholas,J.,et al.GluA1 AMPA受体亚单位基因敲除小鼠长期和短期空间记忆增强:双过程记忆模型的证据。学习和记忆提供了STP可能是STM的一种机制的遗传学证据。
Recent work [Sanderson, D., Good, M.A., Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory, in press] showed that short-term memory (STM) is selectively reduced in GluR1 knockout mice. This raises the possibility that a form of synaptic modification dependent on GluR1 might underlie STM. Studies of synaptic plasticity have shown that stimuli too weak to induce long-term potentiation induce short-term potentiation (STP), a phenomenon that has received little attention. Here we examined several properties of STP and tested the dependence of STP on GluR1. The minimal requirement for inducing STP was examined using a test pathway and a conditioning pathway. Several closely spaced stimuli in the test pathway, forming a single brief burst, were sufficient to induce STP. Thus, STP is likely to be induced by the similar bursts that occur in vivo. STP induction is associative in nature and dependent on the NMDAR. STP decays with two components, a fast component (1.6 ± 0.26 min) and a slower one (19 ± 6.6 min). To test the role of GluR1 in STP, experiments were conducted on GluR1 knockout mice. We found that STP was greatly reduced. These results, taken together with the behavioral work of D. Sanderson et al. [Sanderson, D., Good, M. A, Skelton, K., Sprengel, R., Seeburg, P. H., Nicholas, J., et al. Enhanced long-term and impaired short-term spatial memory in GluA1 AMPA receptor subunit knockout mice: Evidence for a dual-process memory model. Learning and Memory, in press], provide genetic evidence that STP is a likely mechanism of STM.
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期刊: SCIENCE
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