Albin R L, Greenamyre J T
Department of Neurology and Neuroscience Program, University of Michigan, Ann Arbor.
Neurology. 1992 Apr;42(4):733-8. doi: 10.1212/wnl.42.4.733.
The concept of excitotoxicity, neuronal death produced by overstimulation of excitatory amino acid receptors, has become a popular way of explaining the pathogenesis of neuronal death in a variety of acute and chronic neurologic diseases. While there is strong evidence supporting the role of excitotoxicity in acute processes such as hypoxia/ischemia and hypoglycemia, the role of excitotoxicity in chronic neurologic disease is not firmly established. To account for the inter- and intraregional variations in pathology of different neurodegenerative disorders, we suggest two modified forms of the excitotoxic hypothesis in which specific populations of neurons become more vulnerable to excitotoxic insult either by (1) possessing abnormal excitatory amino acid receptor subtypes or (2) being afflicted by any disease process that impairs cellular energy metabolism or otherwise decreases neuronal membrane potential. In these ways, excitotoxicity may be a final common pathway of neuronal death in a variety of neurodegenerative diseases.
兴奋性毒性是指由兴奋性氨基酸受体过度刺激导致神经元死亡的概念，它已成为解释多种急性和慢性神经疾病中神经元死亡发病机制的一种常用方式。虽然有强有力的证据支持兴奋性毒性在诸如缺氧/缺血和低血糖等急性过程中的作用，但兴奋性毒性在慢性神经疾病中的作用尚未得到确凿证实。为了解释不同神经退行性疾病病理学中的区域间和区域内差异，我们提出了两种修正形式的兴奋性毒性假说，即特定神经元群体因以下两种情况而更容易受到兴奋性毒性损伤：（1）拥有异常的兴奋性氨基酸受体亚型，或（2）受到任何损害细胞能量代谢或以其他方式降低神经元膜电位的疾病过程影响。通过这些方式，兴奋性毒性可能是多种神经退行性疾病中神经元死亡的最终共同途径。
