| First Author | Shi J | Year | 2012 |
| Journal | Acta Biochim Biophys Sin (Shanghai) | Volume | 44 |
| Issue | 4 | Pages | 359-66 |
| PubMed ID | 22318715 | Mgi Jnum | J:278364 |
| Mgi Id | MGI:6356250 | Doi | 10.1093/abbs/gms005 |
| Citation | Shi J, et al. (2012) Enhanced learning and memory in GAT1 heterozygous mice. Acta Biochim Biophys Sin (Shanghai) 44(4):359-66 |
| abstractText | gamma-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 behavior 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. |
