Westerberg E, Monaghan D T, Cotman C W, Wieloch T
Neurosci Lett. 1987 Jan 14;73(2):119-24. doi: 10.1016/0304-3940(87)90004-8.
The excitatory amino acid glutamate has been suggested to be an important mediator of the selective CA1 hippocampal damage which follows transient cerebral ischemia. In order to evaluate the possible involvement of altered glutamate receptor regulation in the expression of the delayed neuronal necrosis following ischemia, we have determined the density of glutamate receptor subtypes in the rat hippocampus following transient ischemia. We report a transient reversible decrease in [3H]AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid) binding sites (presumably representing quisqualate receptors) followed by a long term loss of binding at 2 days postischemia which precedes neuronal loss. In contrast, no change was noted in the N-methyl-D-aspartate or kainic acid binding sites over this time period.
兴奋性氨基酸谷氨酸已被认为是短暂性脑缺血后海马CA1区选择性损伤的重要介质。为了评估谷氨酸受体调节改变在缺血后迟发性神经元坏死表达中的可能作用，我们测定了短暂性缺血后大鼠海马中谷氨酸受体亚型的密度。我们报告了[3H]AMPA（α-氨基-3-羟基-5-甲基-4-异恶唑丙酸）结合位点（可能代表quisqualate受体）的短暂可逆性降低，随后在缺血后2天出现结合的长期丧失，这发生在神经元丧失之前。相比之下，在此时间段内N-甲基-D-天冬氨酸或 kainic 酸结合位点没有变化。
