Endomorphin-1 attenuates Aβ42 induced impairment of novel object and object location recognition tasks in mice

被引:10
作者
Zhang, Rui-san [1 ]
Xu, Hong-jiao [1 ]
Jiang, Jin-hong [1 ]
Han, Ren-wen [1 ]
Chang, Min [1 ]
Peng, Ya-li [1 ]
Wang, Yuan [1 ]
Wang, Rui [1 ]
机构
[1] Lanzhou Univ, Sch Basic Med Sci, Key Lab Preclin Study New Drugs Gansu Prov, Lanzhou 730000, Peoples R China
关键词
Endomorphin-1; Amyloid-beta; Alzheimer's disease; Recognition memory; OPIOID RECEPTOR AGONISTS; ALZHEIMERS-DISEASE; MEMORY IMPAIRMENT; A-BETA; PROTEIN; SCOPOLAMINE; PRECURSOR; MODEL; BRAIN; AGGREGATION;
D O I
10.1016/j.brainres.2015.10.028
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
A growing body of evidence suggests that the agglomeration of amyloid-beta (A beta) may be a trigger for Alzheimer's disease (AD). Central infusion of A beta 42 can lead to memory impairment in mice. Inhibiting the aggregation of A beta has been considered a therapeutic strategy for AD. Endomorphin-1 (EM-1), an endogenous agonist of mu-opioid receptors, has been shown to inhibit the aggregation of A beta in vitro. In the present study, we investigated whether EM-1 could alleviate the memory-impairing effects of A beta(42) in mice using novel object recognition (NOR) and object location recognition (OLR) tasks. We showed that co-administration of EM-1 was able to ameliorate A beta(42)-induced amnesia in the lateral ventricle and the hippocampus, and these effects could not be inhibited by naloxone, an antagonist of p-opioid receptors. Infusion of EM-1 or naloxone separately into the lateral ventricle had no influence on memory in the tasks. These results suggested that EM-1 might be effective as a drug for AD preventative treatment by inhibiting A beta aggregation directly as a molecular modifier. (C) 2015 Elsevier B.V. All rights reserved.
引用
收藏
页码:210 / 220
页数:11
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