Roberts E L, Wisotzky D, Chih C P
Geriatric Research, Education, and Clinical Center, Miami VA Medical Center, Miami, FL 33125, USA.
Brain Res. 1998 Apr 27;791(1-2):321-4. doi: 10.1016/s0006-8993(98)00141-3.
We examined whether age-related differences in N-methyl-D-aspartate (NMDA) receptor-mediated neurotoxicity contribute to the increased vulnerability of the aged brain to anoxic damage. In both adult and aged hippocampal slices, NMDA receptor blockade with MK-801 did not affect the onset of anoxic depolarization. MK-801 improved the postanoxic recovery of synaptic transmission by the same percentage in both age groups. Thus, the faster onset of anoxic depolarization and diminished postanoxic recovery of synaptic transmission seen in aged hippocampal slices cannot be attributed to age-related differences in NMDA receptor-mediated neurotoxicity.
我们研究了N-甲基-D-天冬氨酸（NMDA）受体介导的神经毒性方面与年龄相关的差异是否会导致老年大脑对缺氧损伤的易感性增加。在成年和老年海马切片中，用MK-801阻断NMDA受体并不影响缺氧去极化的起始。MK-801在两个年龄组中均以相同的百分比改善了缺氧后突触传递的恢复。因此，在老年海马切片中观察到的缺氧去极化更快起始以及突触传递的缺氧后恢复减弱不能归因于NMDA受体介导的神经毒性方面与年龄相关的差异。
