Amyloid-β injection in rat amygdala alters tau protein but not mRNA expression

被引:19
作者
Chambers, CB
Sigurdsson, EM
Hejna, MJ
Lorens, SA
Lee, JM
Muma, NA
机构
[1] Loyola Univ, Med Ctr, Dept Pathol, Maywood, IL 60153 USA
[2] Loyola Univ, Med Ctr, Dept Pharmacol & Expt Therapeut, Maywood, IL 60153 USA
[3] NYU, Med Ctr, Dept Pathol, New York, NY 10016 USA
关键词
tau; amyloid-beta; RT-PCR; Western blotting; Alzheimer's disease; animal model;
D O I
10.1006/exnr.2000.7325
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Previously we demonstrated local and distant changes in tau protein imnnunoreactivity reminiscent of those seen in Alzheimer's disease (AD) following a unilateral injection of amyloid-beta (A beta)(25-35) into the rat amygdala. To explore the relevance of these findings to AD, we compared the effects of A beta(1-42) to those of A beta(25-35). Injections of both A beta(1-42) and A beta(25-35) into rat amygdala resulted in increased tau-2 immunolabeling in neurons. To determine whether these alterations were due to changes in the expression of tau, we measured tau protein expression by Western blotting and tau mRNA isoform expression by the reverse transcription-polymerase chain reaction in the amygdala, hippocampus, and cerebellum following a unilateral injection of A beta(25-35)-treated (59-69 kDa) compared to the vehicle-treated (67-72 kDa) animals 8 days following treatment. There were no changes in tau mRNA expression in any brain region examined. In this model, just as in AD, there is an increase in tau protein levels without a change in tau mRNA expression, suggesting that A beta peptides may influence tau protein stability in both the rat and the human brain. (C) 2000 Academic Press.
引用
收藏
页码:158 / 170
页数:13
相关论文
共 78 条
[1]   Acute rise in the concentration of free cytoplasmic calcium leads to dephosphorylation of the microtubule-associated protein tau [J].
Adamec, E ;
Mercken, M ;
Beermann, ML ;
Didier, M ;
Nixon, RA .
BRAIN RESEARCH, 1997, 757 (01) :93-101
[2]   STRUCTURE AND NOVEL EXONS OF THE HUMAN-TAU GENE [J].
ANDREADIS, A ;
BROWN, WM ;
KOSIK, KS .
BIOCHEMISTRY, 1992, 31 (43) :10626-10633
[3]   ACCUMULATION OF ABNORMALLY PHOSPHORYLATED-TAU PRECEDES THE FORMATION OF NEUROFIBRILLARY TANGLES IN ALZHEIMERS-DISEASE [J].
BANCHER, C ;
BRUNNER, C ;
LASSMANN, H ;
BUDKA, H ;
JELLINGER, K ;
WICHE, G ;
SEITELBERGER, F ;
GRUNDKEIQBAL, I ;
IQBAL, K ;
WISNIEWSKI, HM .
BRAIN RESEARCH, 1989, 477 (1-2) :90-99
[4]   HYDROGEN-PEROXIDE MEDIATES AMYLOID-BETA PROTEIN TOXICITY [J].
BEHL, C ;
DAVIS, JB ;
LESLEY, R ;
SCHUBERT, D .
CELL, 1994, 77 (06) :817-827
[5]  
BRAMBLETT GT, 1992, LAB INVEST, V66, P212
[6]   ABNORMAL TAU-PHOSPHORYLATION AT SER(396) IN ALZHEIMERS-DISEASE RECAPITULATES DEVELOPMENT AND CONTRIBUTES TO REDUCED MICROTUBULE-BINDING [J].
BRAMBLETT, GT ;
GOEDERT, M ;
JAKES, R ;
MERRICK, SE ;
TROJANOWSKI, JQ ;
LEE, VMY .
NEURON, 1993, 10 (06) :1089-1099
[7]   DEVELOPMENTAL-CHANGES IN TAU-PHOSPHORYLATION - FETAL-TAU IS TRANSIENTLY PHOSPHORYLATED IN A MANNER SIMILAR TO PAIRED HELICAL FILAMENT-TAU CHARACTERISTIC OF ALZHEIMERS-DISEASE [J].
BRION, JP ;
SMITH, C ;
COUCK, AM ;
GALLO, JM ;
ANDERTON, BH .
JOURNAL OF NEUROCHEMISTRY, 1993, 61 (06) :2071-2080
[8]   THE CA2+ INFLUX INDUCED BY BETA-AMYLOID PEPTIDE-25-35 IN CULTURED HIPPOCAMPAL-NEURONS RESULTS FROM NETWORK EXCITATION [J].
BRORSON, JR ;
BINDOKAS, VP ;
IWAMA, T ;
MARCUCCILLI, CJ ;
CHISHOLM, JC ;
MILLER, RJ .
JOURNAL OF NEUROBIOLOGY, 1995, 26 (03) :325-338
[9]   PrP and beta-amyloid fragments activate different neurotoxic mechanisms in cultured mouse cells [J].
Brown, DR ;
Herms, JW ;
Schmidt, B ;
Kretzschmar, HA .
EUROPEAN JOURNAL OF NEUROSCIENCE, 1997, 9 (06) :1162-1169
[10]   BETA-AMYLOID FIBRILS INDUCE TAU-PHOSPHORYLATION AND LOSS OF MICROTUBULE-BINDING [J].
BUSCIGLIO, J ;
LORENZO, A ;
YEH, J ;
YANKNER, BA .
NEURON, 1995, 14 (04) :879-888