中文摘要：

-Aminobutyric 酸(伽马氨基丁酸) 是在中央神经系统的主要禁止的 neurotransmitter。伽马氨基丁酸传播的结束通过膜蛋白质的一个家庭的行动，叫的伽马氨基丁酸 transporters (GAT14 ) 。伽马氨基丁酸系统涉及存储器的调整，这很好被建立。我们的以前的学习显示出老鼠展出了损害马头鱼尾的怪兽依赖者学习和记忆的那同型结合的 GAT1/ 。在鼠标上评估内长的减少的伽马氨基丁酸举起的影响认知行为，学习和异质接合的 GAT1+/ 鼠标的存储器的能力被被动回避范例和莫利斯舞水迷宫检测。洞板范例也被用来在如此的老鼠在焦虑相关的行为或探索行为测量变化。作为 synaptic 粘性的一种形式，长期的 potentiation 在老鼠被记录海马趾的 CA1 区域。我们发现了显示的老鼠增加了的那 GAT1+/ 学习并且记忆，减少的像焦虑的行为，和与野类型、同型结合的 GAT1/ 老鼠相比的最高的 synaptic 粘性。我们的结果建议在 GAT1 活动的中等减小引起在鼠标学习和记忆的改进。

英文摘要：

γ-Aminobutyric acid （GABA） is the major inhibitory neurotransmitter in the central nervous system. The termination of GABA transmission is through the action of a family of membrane proteins, called GABA transporters （GAT1-4）. It is well established that GABA system is involved in the modulation of memory. Our previous study showed that homozygous GAT1^-/- mice exhibited impaired hippocampus-dependent learning and memory. To evaluate the impact of endogenous reduced GABA reuptake on mice cognitive behaviors, the ability of learning and memory of heterozygous GAT1^＋/- mice was detected by the passive avoidance paradigm and Morris water maze. The hole board paradigm was also used to measure changes in anxiety-related behavior or exploratory behav- ior in such mice. As one form of synaptic plasticity, long- term potentiation was recorded in the mouse hippocampal CA1 area. We found that GAT1^＋/- mice displayed increased learning and memory, decreased anxiety-like behaviors, and highest synaptic plasticity compared with wild-type and homozygous GAT1^-/- mice. Our results suggest that a moderate reduction in GAT1 activity causes the enhancement of learning and memory in mice.