High salt diet impairs memory‐related synaptic plasticity via increased oxidative stress and suppressed synaptic protein expression. Issue 10 (15th August 2017)

• Record Type: Journal Article
• Authors: Ge, Qian; Wang, Zhengjun; Wu, Yuwei; Huo, Qing; Qian, Zhaoqiang; Tian, Zhongmin; Ren, Wei; Zhang, Xia; Han, Jing
• Is Part Of: Molecular nutrition & food research. Volume 61:Issue 10(2017)
• Page Start: n/a
• Page End: n/a
• Publication Date: 2017-08-15
• Subjects: High salt -- Memory -- Oxidative stress -- Synaptic plasticity -- Synaptic protein; Food -- Biotechnology -- Periodicals; Food -- Microbiology -- Periodicals; Nutrition -- Periodicals; Food -- Toxicology -- Periodicals; Nutrition -- Periodicals; Food Microbiology -- Periodicals; Food Technology -- Periodicals; Molecular Biology -- Periodicals; 664.0705
• DOI: 10.1002/mnfr.201700134
• Languages: English
• ISSNs: 1613-4125

Abstract

Abstract : 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. Abstract : Possible mechanisms underlying HS‐induced impairment in cognition and neuroplasticity. An HS diet in mice could impair both short‐ and long‐term memory, probably due to disturbed synaptic plasticity in the hippocampus. The candidate mechanisms responsible for these neurological disorders may include oxidative stress (OS) and suppressed expression of synaptic proteins or neurotrophins.