High salt diet impairs memory-related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression

被引:39
|
作者
Ge, Qian [1 ]
Wang, Zhengjun [2 ]
Wu, Yuwei [1 ]
Huo, Qing [1 ]
Qian, Zhaoqiang [1 ]
Tian, Zhongmin [2 ]
Ren, Wei [1 ]
Zhang, Xia [1 ]
Han, Jing [1 ]
机构
[1] Shaanxi Normal Univ, Key Lab Modern Teaching Technol, Xian, Shaanxi, Peoples R China
[2] Xi An Jiao Tong Univ, Sch Life Sci & Technol, Key Lab Biomed Informat Engn, Minist Educ, Xian, Shaanxi, Peoples R China
基金
中国国家自然科学基金;
关键词
High salt; Memory; Oxidative stress; Synaptic plasticity; Synaptic protein; LONG-TERM POTENTIATION; HIPPOCAMPAL NEUROGENESIS; SENSITIVE HYPERTENSION; COGNITIVE IMPAIRMENT; BLOOD-PRESSURE; EARLY-LIFE; RECEPTOR; ACTIVATION; MICE; NUCLEUS;
D O I
10.1002/mnfr.201700134
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
Scope: A high salt (HS) diet is detrimental to cognitive function, in addition to having a role in cardiovascular disorders. However, the method by which an HS diet impairs cognitive functions such as learning and memory remains open. Methods and results: In this study, we found that mice on a 7 week HS diet demonstrated disturbed short-term memory in an object-place recognition task, and both 4 week and 7 week HS treatments impaired long-term memory, as evidenced in a fear conditioning test. Mechanistically, the HS diet inhibited memory-related long-term potentiation (LTP) in the hippocampus, while also increasing the levels of reactive oxygen species (ROS) in hippocampal cells and downregulating the expression of synapsin I, synaptophysin, and brain-derived neurotrophic factor in specific encephalic region. Conclusion: This suggests that oxidative stress or synaptic protein/neurotrophin deregulation was involved in the HS diet-induced memory impairment. Thus, the present study provides novel insights into the mechanisms of memory impairment caused by excessive dietary salt, and underlined the importance of controlling to salt absorb quantity.
引用
收藏
页数:11
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