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Arc/Arg3.1对于突触可塑性和记忆的巩固至关重要。

Arc/Arg3.1 is essential for the consolidation of synaptic plasticity and memories.

作者信息

Plath Niels, Ohana Ora, Dammermann Björn, Errington Mick L, Schmitz Dietmar, Gross Christina, Mao Xiaosong, Engelsberg Arne, Mahlke Claudia, Welzl Hans, Kobalz Ursula, Stawrakakis Anastasia, Fernandez Esperanza, Waltereit Robert, Bick-Sander Anika, Therstappen Eric, Cooke Sam F, Blanquet Veronique, Wurst Wolfgang, Salmen Benedikt, Bösl Michael R, Lipp Hans-Peter, Grant Seth G N, Bliss Tim V P, Wolfer David P, Kuhl Dietmar

机构信息

Molecular Neurobiology, Department of Biology-Chemistry-Pharmacy, Freie Universität Berlin, 14195 Berlin, Germany.

出版信息

Neuron. 2006 Nov 9;52(3):437-44. doi: 10.1016/j.neuron.2006.08.024.

Abstract

Arc/Arg3.1 is robustly induced by plasticity-producing stimulation and specifically targeted to stimulated synaptic areas. To investigate the role of Arc/Arg3.1 in synaptic plasticity and learning and memory, we generated Arc/Arg3.1 knockout mice. These animals fail to form long-lasting memories for implicit and explicit learning tasks, despite intact short-term memory. Moreover, they exhibit a biphasic alteration of hippocampal long-term potentiation in the dentate gyrus and area CA1 with an enhanced early and absent late phase. In addition, long-term depression is significantly impaired. Together, these results demonstrate a critical role for Arc/Arg3.1 in the consolidation of enduring synaptic plasticity and memory storage.

摘要

Arc/Arg3.1 可由产生可塑性的刺激强烈诱导,并特异性定位于受刺激的突触区域。为了研究 Arc/Arg3.1 在突触可塑性以及学习和记忆中的作用,我们培育出了 Arc/Arg3.1 基因敲除小鼠。尽管这些动物的短期记忆完好无损,但它们无法为隐性和显性学习任务形成持久记忆。此外,它们在齿状回和 CA1 区的海马长时程增强呈现双相改变,早期增强而晚期缺失。另外,长时程抑制也显著受损。这些结果共同表明,Arc/Arg3.1 在持久突触可塑性的巩固和记忆存储中起关键作用。

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