Dual response of BDNF to sublethal concentrations of β-amyloid peptides in cultured cortical neurons

被引:35
作者
Aliaga, E. [3 ]
Silhol, M. [1 ,2 ,3 ]
Bonneau, N. [1 ,2 ,3 ]
Maurice, T. [1 ,2 ,3 ]
Arancibia, S. [1 ,2 ,3 ]
Tapia-Arancibia, L. [1 ,2 ,3 ]
机构
[1] Univ Montpellier 2, INSERM, U710, F-34095 Montpellier 5, France
[2] EPHE, F-75007 Paris, France
[3] Univ Valparaiso, Fac Ciencias, Dept Fisiol, Ctr Neurobiol & Plasticidad Desarrollo, Valparaiso, Chile
关键词
Alzheimer's disease; Cultured cortical neurons; Beta-amyloids; BDNF; proBDNF; TrkB receptors; TrkB T1 receptors; p75(NGFR); BDNF transcripts; P-CREB; TRKB NEUROTROPHIN RECEPTORS; TYROSINE KINASE RECEPTOR; MESSENGER-RNA EXPRESSION; INDUCED ARC EXPRESSION; ALZHEIMERS-DISEASE; TRANSGENIC MICE; IN-VIVO; OXIDATIVE STRESS; PARIETAL CORTEX; FULL-LENGTH;
D O I
10.1016/j.nbd.2009.10.004
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Beta-amyloid (A beta) deposition is one important pathological hallmark in Alzheimer's disease (AD). However. low levels of A beta may modify critical endogenous protection systems before neurodegeneration occurs. We examined the time-course effect of sublethal concentrations of A beta on total BDNF (panBDNF), BDNF transcripts (I, II, IV and VI). trkB.FL. trkB.T1 and p75(NGFR) mRNA expression in cultured cortical neurons We have shown that A beta exhibited a dual response on BDNF mRNA, i.e an increase at short times (3-5 h) and a dramatic decrease at longer times (24 or 48 h). The early increase in BDNF expression seems to be driven by increased expression of transcripts I and IV. The BDNF drop was specific since did not occur for other mRNAs examined. The BDNF protein content showed a similar profile but did not follow the dramatic reduction as its encoding mRNA. These observations may help to explain cognitive deficits observed at initial stages of AD. (C) 2009 Elsevier Inc. All rights reserved.
引用
收藏
页码:208 / 217
页数:10
相关论文
共 90 条
[61]   Neurotoxic effect of oligomeric and fibrillar species of amyloid-beta peptide 1-42: Involvement of endoplasmic reticulum calcium release in oligomer-induced cell death [J].
Resende, R. ;
Ferreiro, E. ;
Pereira, C. ;
De Oliveira, C. Resende .
NEUROSCIENCE, 2008, 155 (03) :725-737
[62]   Truncated TrkB-T1 mediates neurotrophin-evoked calcium signalling in glia cells [J].
Rose, CR ;
Blum, R ;
Pichler, B ;
Lepier, A ;
Kafitz, KW ;
Konnerth, A .
NATURE, 2003, 426 (6962) :74-78
[63]  
Rozen S, 2000, Methods Mol Biol, V132, P365
[64]   Transgenic mice overexpressing truncated trkB neurotrophin receptors in neurons show increased susceptibility to cortical injury after focal cerebral ischemia [J].
Saarelainen, T ;
Lukkarinen, JA ;
Koponen, S ;
Gröhn, OHJ ;
Jolkkonen, J ;
Koponen, E ;
Haapasalo, A ;
Alhonen, L ;
Wong, G ;
Koistinaho, J ;
Kauppinen, RA ;
Castrén, E .
MOLECULAR AND CELLULAR NEUROSCIENCE, 2000, 16 (02) :87-96
[65]  
Saarelainen T, 2000, SYNAPSE, V38, P102, DOI 10.1002/1098-2396(200010)38:1<102::AID-SYN11>3.0.CO
[66]  
2-K
[67]   BDNF gene can be activated by Ca2+ signals without involvement of de Novo AP-1 synthesis [J].
Sano, K ;
Nanba, H ;
Tabuchi, A ;
Tsuchiya, T ;
Tsuda, M .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1996, 229 (03) :788-793
[68]   Identification of a signaling pathway involved in calcium regulation of BDNF expression [J].
Shieh, PB ;
Hu, SC ;
Bobb, K ;
Timmusk, T ;
Ghosh, A .
NEURON, 1998, 20 (04) :727-740
[69]   Spatial memory training modifies the expression of brain-derived neurotrophic factor tyrosine kinase receptors in young and aged rats [J].
Silhol, M. ;
Arancibia, S. ;
Maurice, T. ;
Tapia-Arancibia, L. .
NEUROSCIENCE, 2007, 146 (03) :962-973
[70]   Age-related changes in brain-derived neurotrophic factor and tyrosine kinase receptor isoforms in the hippocampus and hypothalamus in male rats [J].
Silhol, M ;
Bonnichon, V ;
Rage, F ;
Tapia-Arancibia, L .
NEUROSCIENCE, 2005, 132 (03) :613-624