突触前活性区蛋白RIM1α对正常学习和记忆至关重要。
The presynaptic active zone protein RIM1alpha is critical for normal learning and memory.
作者信息
Powell Craig M, Schoch Susanne, Monteggia Lisa, Barrot Michel, Matos Maria F, Feldmann Nicole, Südhof Thomas C, Nestler Eric J
机构信息
Department of Psychiatry, The University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.
出版信息
Neuron. 2004 Apr 8;42(1):143-53. doi: 10.1016/s0896-6273(04)00146-1.
Abstract
The active zone protein RIM1alpha is required both for maintaining normal probability of neurotransmitter release and for long-term presynaptic potentiation at brain synapses. We now demonstrate that RIM1alpha(-/-) mice exhibit normal coordination and anxiety-related behaviors but display severely impaired learning and memory. Mice with a synaptotagmin 1 mutation, which selectively lowers release probability, and mice with Rab3A deletion, which selectively abolishes presynaptic long-term potentiation, do not exhibit this abnormality. Our data suggest that a decrease in release probability or a loss of presynaptic LTP alone is not sufficient to cause major behavioral alterations, but the combination of presynaptic abnormalities in RIM1alpha(-/-) mice severely alters learning and memory.
摘要
活性区蛋白RIM1α对于维持神经递质释放的正常概率以及大脑突触的长期突触前增强都是必需的。我们现在证明，RIM1α基因敲除小鼠表现出正常的协调性和与焦虑相关的行为，但学习和记忆能力严重受损。具有突触结合蛋白1突变（选择性降低释放概率）的小鼠以及具有Rab3A基因缺失（选择性消除突触前长期增强）的小鼠均未表现出这种异常。我们的数据表明，仅释放概率的降低或突触前长时程增强的丧失不足以引起主要的行为改变，但RIM1α基因敲除小鼠中突触前异常的组合会严重改变学习和记忆。
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本文引用的文献
1
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Cell. 2003 Oct 3;115(1):49-60. doi: 10.1016/s0092-8674(03)00727-x.
2
Genetic neuroscience of mammalian learning and memory.哺乳动物学习与记忆的遗传神经科学
Philos Trans R Soc Lond B Biol Sci. 2003 Apr 29;358(1432):787-95. doi: 10.1098/rstb.2002.1243.
3
Spatial, contextual and working memory are not affected by the absence of mossy fiber long-term potentiation and depression.空间记忆、情境记忆和工作记忆不受苔藓纤维长时程增强和长时程抑制缺失的影响。
Behav Brain Res. 2003 Jan 22;138(2):215-23. doi: 10.1016/s0166-4328(02)00243-7.
4
Genetic approaches to molecular and cellular cognition: a focus on LTP and learning and memory.分子与细胞认知的遗传学方法：聚焦于长时程增强以及学习与记忆
Annu Rev Genet. 2002;36:687-720. doi: 10.1146/annurev.genet.36.062802.091007. Epub 2002 Sep 12.
5
GABA-A receptor complex and memory processes.γ-氨基丁酸A受体复合物与记忆过程。
Curr Top Med Chem. 2002 Aug;2(8):841-51. doi: 10.2174/1568026023393552.
6
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Trends Neurosci. 2002 Jul;25(7):329-32. doi: 10.1016/s0166-2236(02)02193-8.
7
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8
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9
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Nature. 2002 Jan 17;415(6869):277-8. doi: 10.1038/415277a.
10
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Annu Rev Neurosci. 2001;24:897-931. doi: 10.1146/annurev.neuro.24.1.897.
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