Netrin-1 improves the amyloid-β-mediated suppression of memory and synaptic plasticity

被引:30
作者
Shabani, Mohammad [1 ]
Haghani, Masoud [2 ,3 ]
Tazangi, Parisa Esmaeili [2 ]
Bayat, Mahnaz [4 ]
Moosavi, Seyed Mostafa Shid [2 ]
Ranjbar, Hoda [1 ]
机构
[1] Kerman Univ Med Sci, Neuropharmacol Inst, Neurosci Res Ctr, Kerman, Iran
[2] Shiraz Univ Med Sci, Dept Physiol, Shiraz 713651689, Iran
[3] Shiraz Univ Med Sci, Histomorphometry & Stereol Res Ctr, Shiraz, Iran
[4] Shiraz Univ Med Sci, Dept Physiol, Int Branch, Shiraz, Iran
关键词
Beta amyloid; Netrin-1; Long-term potentiation; Alzheimer's disease; LONG-TERM POTENTIATION; RECEPTOR ACTIVATION; PRECURSOR PROTEIN; LATE-PHASE; NEURONS; ISCHEMIA; TRANSMISSION; INHIBITION; EXPRESSION; APOPTOSIS;
D O I
10.1016/j.brainresbull.2017.03.015
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
The aim of this study was to investigate the effects of netrin-1 (NT-1) on amyloid-beta (A(3) induced impairments in learning-memory and synaptic plasticity. The NT-1 or its vehicle was administered four times into the A beta+ NT or A beta 3 + V groups, respectively. The A beta+ SNT group received a single dose of NT-1. The A beta+ HNT group received heat-inactivated NT-1. For the learning-memory and synaptic plasticity assessment, field potentials recording and behavioral experiment were used. Bilateral injection of A beta(1-42) inhibits induction of long-term potentiation (LTP) and decreased memory performance in all the behavioral tasks. However, only by repeated injection of NT-1, significant recovery of LTP and memory was seen. Although, the delivery of HFS to A beta+ NT group recovered EPSP slope of the maintenance phase when compared with A beta + V, but it failed to recover the induction phase. It can be assumed that NT-1 may have regulatory effects on the synthesis of key proteins and/or structural changes that are responsible for LTP induction, since the protein synthesis and/or structural changes are required for the maintenance phase of LTP.
引用
收藏
页码:107 / 116
页数:10
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