期刊
NEUROPHARMACOLOGY
卷 75, 期 -, 页码 213-222出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuropharm.2013.08.009
关键词
Ceftriaxone; GLT-1; AQP4; Memory; Long-term potentiation
资金
- National Natural Science Foundation of China (NSFC) [81222048]
- National Basic Research Program of China (973 Program) [2013CB531303]
- Key Project of NSFC [30930104]
- International Science & Technology Cooperation Program of China [2011DFA32670]
Aquaporin-4 (AQP4) is the predominant water channel protein in the mammalian brain, and is mainly expressed in astrocytes. Besides its important role in water transport across the blood-brain barrier, our present study demonstrated that AQP4 deficiency impaired hippocampal long-term potentiation (LTP) and hippocampus-dependent memory formation, accompanied by the increase in extracellular glutamate concentration and N-methyl-D-aspartate (NMDA) receptor-mediated currents in hippocampal dentate gyros (DG) region. The impairment of LTP and memory formation of AQP4 knockout (KO) mice was mediated by the downregulation of glutamate transporter-1 (GLT-1) expression/function, since it can be rescued by beta-lactam antibiotic ceftriaxone (Cef), a potent GLT-1 stimulator. These results suggest that AQP4 functions as the modulator of synaptic plasticity and memory, and chronic Cef treatment rescues hippocampal memory deficit induced by AQP4 knockout. (C) 2013 Elsevier Ltd. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据