Ludolph A C, Riepe M, Ullrich K
Department of Epileptology, University of Bonn, Germany.
J Inherit Metab Dis. 1993;16(4):716-23. doi: 10.1007/BF00711903.
There is increasing evidence that the neurotoxic effects of excitatory amino acids and their analogues are part of the pathogenesis of neuronal degeneration in acute and chronic neurological disease. Recent studies indicate that activation of excitatory amino acid receptors is also induced in the mechanism of neuronal damage induced by impairment of cellular energy metabolism. This article briefly summarizes the evidence for the presence of such a mechanism and discusses metabolic diseases in which excitatory amino acids alone or in combination with energy deficiency could play a pathogenetic role. In these and other metabolic diseases, antagonists to excitatory amino acid receptors may offer a therapeutic opportunity; however, there are potential limits that may prevent chronic use.
越来越多的证据表明，兴奋性氨基酸及其类似物的神经毒性作用是急慢性神经疾病中神经元变性发病机制的一部分。最近的研究表明，细胞能量代谢受损所诱导的神经元损伤机制中也会诱导兴奋性氨基酸受体的激活。本文简要总结了存在这种机制的证据，并讨论了单独或与能量缺乏共同作用可能发挥致病作用的兴奋性氨基酸的代谢疾病。在这些及其他代谢疾病中，兴奋性氨基酸受体拮抗剂可能提供治疗机会；然而，可能存在一些潜在限制，妨碍其长期使用。
