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 leaing and memory.To evaluate the impact of endogenous reduced GABA reuptake on mice cognitive behaviors,the ability of leaing 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 behavior in such mice.As one form of synaptic plasticity,longterm potentiation was recorded in the mouse hippocampal CA1 area.We found that GAT1+/- mice displayed increased leaing 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 leaing and memory in mice.