Apoptotic mechanisms in normal brain plasticity: Caspase-3 and long-term potentiation

被引：0
作者：
Gulyaeva, NV [1 ]
机构：
[1] Russian Acad Sci, Inst Higher Nervous Act & Neurophysiol, Dept Funct Biochem, Moscow 117865, Russia
来源：
ZHURNAL VYSSHEI NERVNOI DEYATELNOSTI IMENI I P PAVLOVA | 2004年 / 54卷 / 04期
关键词：
neuroplasticity; apoptosis; caspase-3; long-term potentiation; hippocampus; CA1;
D O I：
暂无
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
The analysis of recent data indicates that a few enzymes that have been recognized as "apoptotic" so far may be involved in important cellular processes not related to cell death in the brain. For example, it can be demonstrated that caspase-3, an "apoptotic" enzyme that is active in neurons is necessary for normal neuroplasticity. Here we discuss the involvement of caspase-3 in long-term potentiation phenomenon. Proteins that are key players of molecular mechanisms of long-term potentiation induction and maintenance are also caspase-3 substrates. A concept on a new mechanism of synaptic plasticity modulation involving caspase-3 has been formulated postulating a specific role of caspase-3 in normal brain functioning.
引用
收藏
页码：437 / 447
页数：11
相关论文
共 129 条
  • [1] Adam-Klages S, 1998, J IMMUNOL, V161, P5687
  • [2] Expression and subcellular localization of multifunctional calmodulin-dependent protein kinases-I, -II and -IV are altered in rat hippocampal CA1 neurons after induction of long-term potentiation
    Ahmed, BY
    Yamaguchi, F
    Tsumura, T
    Gotoh, T
    Sugimoto, K
    Tai, YJ
    Konishi, R
    Kobayashi, R
    Tokuda, M
    [J]. NEUROSCIENCE LETTERS, 2000, 290 (02) : 149 - 153
  • [3] MELITTIN ENHANCES EXCITATORY AMINO-ACID RELEASE AND AMPA-STIMULATED CA-45(2+) INFLUX IN CULTURED NEURONS
    ARONICA, E
    CASABONA, G
    GENAZZANI, AA
    CATANIA, MV
    CONTESTABILE, A
    VIRGILI, M
    NICOLETTI, F
    [J]. BRAIN RESEARCH, 1992, 586 (01) : 72 - 77
  • [4] Distinct roles of two intracellular phospholipase A2s in fatty acid release in the cell death pathway -: Proteolytic fragment of type IVA cytosolic phospholipase A2α inhibits stimulus-induced arachidonate release, whereas that of type VICa2+-independent phospholipase A2 augments spontaneous fatty acid release
    Atsumi, G
    Murakami, M
    Kojima, K
    Hadano, A
    Tajima, M
    Kudo, I
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 2000, 275 (24) : 18248 - 18258
  • [5] A short cytoplasmic domain of the amyloid precursor protein induces apoptosis in vitro and in vivo
    Bertrand, E
    Brouillet, E
    Caillé, I
    Bouillot, C
    Cole, GM
    Prochiantz, A
    Allinquant, B
    [J]. MOLECULAR AND CELLULAR NEUROSCIENCE, 2001, 18 (05) : 503 - 511
  • [6] A SYNAPTIC MODEL OF MEMORY - LONG-TERM POTENTIATION IN THE HIPPOCAMPUS
    BLISS, TVP
    COLLINGRIDGE, GL
    [J]. NATURE, 1993, 361 (6407) : 31 - 39
  • [7] Transforming growth factor β induces caspase 3-independent cleavage of αII-spectrin (α-fodrin) coincident with apoptosis
    Brown, TL
    Patil, S
    Cianci, CD
    Morrow, JS
    Howe, PH
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (33) : 23256 - 23262
  • [8] Cytokine production in T lymphocyte-microglia interaction is attenuated by glatiramer acetate: a mechanism for therapeutic efficacy in multiple sclerosis
    Chabot, S
    Yong, FP
    Le, DM
    Metz, LM
    Myles, T
    Yong, VW
    [J]. MULTIPLE SCLEROSIS JOURNAL, 2002, 8 (04) : 299 - 306
  • [9] Chan SL, 1999, J NEUROSCI RES, V58, P167, DOI 10.1002/(SICI)1097-4547(19991001)58:1<167::AID-JNR16>3.3.CO
  • [10] 2-B
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