Neuroprotection, excitotoxicity and NMDA antagonists

被引:60
作者
Gagliardi, RJ [1 ]
机构
[1] Santa Casa Sao Paulo, Fac Ciencias Med, Dept Med, Disciplina Neurol, Sao Paulo, Brazil
关键词
neuroprotection; excitotoxicity; NMDA antagonists; stroke;
D O I
10.1590/S0004-282X2000000300030
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Purpose - To analyze the main aspects of neuroprotection and excitotoxicity. Discussion - This is a significant theory on the pathophysiology of cerebral ischemia; it is based on the release of excitatory aminoacid (EAA), mainly glutamate, The sequence starts with a decrease of the blood flow and ends in neuronal death. The main stages of this reaction are herein presented and discussed. An in depth study of the effects of the excessive intracellular calcium is undertaken. Neuroprotectors (NP) are a group of drugs that reduce the excitotoxicity, opposing the excessive release of EAA and its intracellular effects. Neuroprotectors represent a rational approach to stroke treatment and offer a number of potential advantages. They prevent or limit ischemia-induced damage. Conclusion - There are many experimental and clinical NP trials. A minimum of 800 trials are currently under study worldwide. The most important NP subgroups are: N-methyl D-aspartate (NMDA) antagonists, gamma-amino butyric acid (GABA) agonists, amino-hydroxy-methyl-isoxalone propionic acid (AMPA) antagonists, reducers of intracellular Ca++ inhibitors of nitric oxide modulation pathway free radicals scavengers, sodium channel antagonists, glutamate release inhibitor; growth factors, hypothermia and potassium channel activators.
引用
收藏
页码:583 / 588
页数:6
相关论文
共 25 条
  • [1] BUCHAN AM, 1990, CEREBROVAS BRAIN MET, V2, P1
  • [2] Sodium influx plays a major role in the membrane depolarization induced by oxygen and glucose deprivation in rat striatal spiny neurons
    Calabresi, P
    Marfia, GA
    Centonze, D
    Pisani, A
    Bernardi, G
    [J]. STROKE, 1999, 30 (01) : 171 - 178
  • [3] CHOI DW, 1990, CEREBROVAS BRAIN MET, V2, P105
  • [4] Choi DW, 1996, STROKE, V27, P2130
  • [5] CHOI DW, 1990, ANNU REV NEUROSCI, V13, P171, DOI 10.1146/annurev.neuro.13.1.171
  • [6] Long-lasting neuroprotective effect of postischemic hypothermia and treatment with an anti-inflammatory/antipyretic drug - Evidence for chronic encephalopathic processes following ischemia
    Coimbra, C
    Drake, M
    BorisMoller, F
    Wieloch, T
    [J]. STROKE, 1996, 27 (09) : 1578 - 1585
  • [7] Duration of glutamate release after acute ischemic stroke
    Davalos, A
    Castillo, J
    Serena, J
    Noya, M
    [J]. STROKE, 1997, 28 (04) : 708 - 710
  • [8] NITRIC-OXIDE AND THE CEREBRAL-CIRCULATION
    FARACI, FM
    BRIAN, JE
    [J]. STROKE, 1994, 25 (03) : 692 - 703
  • [9] FLAVIN MP, 1996, J NEUROPATH EXP NEUR, V39, P34
  • [10] ACIDOSIS REDUCES NMDA RECEPTOR ACTIVATION, GLUTAMATE NEUROTOXICITY, AND OXYGEN-GLUCOSE DEPRIVATION NEURONAL INJURY IN CORTICAL CULTURES
    GIFFARD, RG
    MONYER, H
    CHRISTINE, CW
    CHOI, DW
    [J]. BRAIN RESEARCH, 1990, 506 (02) : 339 - 342