Cultured neurons expressing phosphorylated tau are more resistant to apoptosis induced by NMDA or serum deprivation

被引:49
作者
Lesort, M [1 ]
Blanchard, C [1 ]
Yardin, C [1 ]
Esclaire, F [1 ]
Hugon, J [1 ]
机构
[1] FAC MED LIMOGES,DEPT CELL BIOL & HISTOL,CNRS 1485,NEUROBIOL & CELLULAR PATHOL UNIT,F-87025 LIMOGES,FRANCE
来源
MOLECULAR BRAIN RESEARCH | 1997年 / 45卷 / 01期
关键词
apoptosis; excitotoxicity; serum deprivation; phosphorylated tau; primary neuronal culture;
D O I
10.1016/S0169-328X(96)00284-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Apoptosis is a programmed cell death that occurs during the development of the nervous system and in neurodegenerative disorders. Tau protein is a cytoskeletal component that promotes microtubule polymerization and stabilization. Apoptosis was induced in primary neuronal cultures by a prolonged exposure (16 h) to the NMDA (N-methyl-D-aspartate 20 mu M) or by serum deprivation. The percentages of apoptotic neurons expressing phosphorylated tau (AT8) immunoreactivity are comparable in control and NMDA-exposed cultures (7.5 +/- 1.9 and 6.9 +/- 1.9%, respectivelly). At the opposite, the percentage of apoptotic neurons expressing de-phosphorylated tau (tau1) immunolabellings is dramatically increased in NMDA-treated cultures (x2.3 of controls). Similar results were also observed 48 h after serum deprivation. These results demonstrate in vitro that under these conditions, resistant and sensitive cortical neurons to apoptosis can be partly differentiated according to their phosphorylated tau immunoreactivities.
引用
收藏
页码:127 / 132
页数:6
相关论文
共 30 条
[1]  
Atabay C, 1996, J NEUROSCI RES, V43, P465
[2]   APOPTOSIS AND NECROSIS - 2 DISTINCT EVENTS INDUCED, RESPECTIVELY, BY MILD AND INTENSE INSULTS WITH N-METHYL-D-ASPARTATE OR NITRIC-OXIDE SUPEROXIDE IN CORTICAL CELL-CULTURES [J].
BONFOCO, E ;
KRAINC, D ;
ANKARCRONA, M ;
NICOTERA, P ;
LIPTON, SA .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1995, 92 (16) :7162-7166
[3]   EXCITOTOXIC CELL-DEATH [J].
CHOI, DW .
JOURNAL OF NEUROBIOLOGY, 1992, 23 (09) :1261-1276
[4]   Modifications of neuronal phosphorylated tau immunoreactivity induced by NMDA toxicity [J].
Couratier, P ;
Lesort, M ;
Sindou, P ;
Esclaire, F ;
Yardin, C ;
Hugon, J .
MOLECULAR AND CHEMICAL NEUROPATHOLOGY, 1996, 27 (03) :259-273
[5]   THE PHOSPHORYLATION STATE OF THE MICROTUBULE-ASSOCIATED PROTEIN TAU AS AFFECTED BY GLUTAMATE, COLCHICINE AND BETA-AMYLOID IN PRIMARY RAT CORTICAL NEURONAL CULTURES [J].
DAVIS, DR ;
BRION, JP ;
COUCK, AM ;
GALLO, JM ;
HANGER, DP ;
LADHANI, K ;
LEWIS, C ;
MILLER, CCJ ;
RUPNIAK, T ;
SMITH, C ;
ANDERTON, BH .
BIOCHEMICAL JOURNAL, 1995, 309 :941-949
[6]  
DAWSON TM, 1993, P NATL ACAD SCI USA, V90, P6808
[7]  
FERRER I, 1995, ACTA NEUROPATHOL, V90, P504
[8]   Biochemistry of cell death [J].
Fraser, A ;
McCarthy, N ;
Evan, GI .
CURRENT OPINION IN NEUROBIOLOGY, 1996, 6 (01) :71-80
[9]   PREVENTION OF PROGRAMMED CELL-DEATH OF SYMPATHETIC NEURONS BY THE BCL-2 PROTOONCOGENE [J].
GARCIA, I ;
MARTINOU, I ;
TSUJIMOTO, Y ;
MARTINOU, JC .
SCIENCE, 1992, 258 (5080) :302-304
[10]   MONOCLONAL-ANTIBODY AT8 RECOGNIZES TAU-PROTEIN PHOSPHORYLATED AT BOTH SERINE-202 AND THREONINE-205 [J].
GOEDERT, M ;
JAKES, R ;
VANMECHELEN, E .
NEUROSCIENCE LETTERS, 1995, 189 (03) :167-170