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谷氨酸和N-甲基-D-天冬氨酸(NMDA)受体介导的兴奋性毒性作用是引起新生儿缺氧缺血性脑损伤的病理基础之一。在脑缺氧缺血时,未成熟的NMDA受体和神经突触更易被细胞间隙堆积的谷氨酸激活,引起致死性Ca~(2+)内流,导致神经细胞变性、坏死或凋亡。介绍近年对谷氨酸和NMDA受体的研究进展,阐述NMDA受体和神经突触在发育过程中的特点,探讨其介导新生儿缺氧缺血性脑损伤的可能机制,并对临床治疗和保护措施作一展望。
Glutamate and N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity is one of the pathological basis of neonatal hypoxic-ischemic brain damage. During hypoxic-ischemic brain injury, immature NMDA receptors and synapses are more activated by glutamate accumulation in the interstitial spaces, leading to lethal Ca 2+ influx leading to degeneration, necrosis or apoptosis of nerve cells . In recent years, the research progress of glutamate and NMDA receptor is introduced. The characteristics of NMDA receptor and synapse during development are expounded, and the possible mechanism of NMDA receptor and synapse in developing neonatal hypoxic-ischemic brain damage is introduced. And protection measures for a look.