The role of amino acid neurotransmitters in focal cerebral ischemia

近年来，神经递质在缺血性神经元损伤中的作用已被广泛认识。特别是兴奋性氨基酸神经递质，如谷氨酸和天冬氨酸的作用，引起注意。本研究探讨了大鼠局灶性脑缺血后慢性期神经元的变化、缺血后神经递质的变化、兴奋性氨基酸受体非竞争性拮抗剂MK-801对局灶性脑缺血模型的影响以及局灶性脑缺血后行为学的变化。在神经病理学研究中，我们特别关注同侧丘脑和同侧黑质的延迟变化。在大鼠大脑中动脉阻断模型中，在大脑中动脉阻断后6个月，同侧丘脑和同侧黑质均出现明显的萎缩变化。缺血侧这些区域的变性和萎缩很可能是由于神经递质介导的 关于我们 细胞死亡这些结果表明，局灶性脑缺血后，在远处的非缺血区的迟发性神经元损失。这些神经病理学的变化，在同侧丘脑和黑质最初发现在大鼠大脑中动脉闭塞模型同样发生在大脑中动脉领域的脑梗死的临床病例。其次，我们研究了MK-801对局灶性脑缺血模型的影响。因此，治疗组的大脑皮层梗死面积显著减少。结果表明，兴奋性毒性机制可能是导致皮层神经元缺血性损伤的重要机制。第三，研究大鼠局灶性脑缺血后的行为学变化。与假手术动物相比，MCA闭塞动物在一次试验中的被动回避反应和主动回避反应中表现出显著的学习行为障碍。在主动回避任务中，学习障碍与组织损伤密切相关，而在被动回避任务中没有观察到这种相关性。少

Recently, the potential role of neurotransmitters on ischemic neuronal injury has come to be widely realized. In particular, the role of excitatory amino acids neurotransmitters, such as glutamate and aspartate, atracts attention. In this study, we examined neuronal alterations in a chronic phase after focal cerebral damage, changes of neurotransmitters after ischemia, the effect of a non-competitive antagonist of excitatory amino acid receptor, MK-801, on focal cerebral ischemia model in rats, and behavioral changes after focal cerebral ischemia. In the neuropathological study, we particularly focused on the delayed changes in the ipsilateral thalamus and also those in the ipsilateral substantia nigra. In the rat MCA occlusion model, marked atrophic chenges were obserbed in the ipsilateral thalamus and also ipsilateral substantia nigra at 6 months following MCA occlusion. The degeneration and shrinkage of these areas on the ischemic side is most likely due to neurotransmitter-mediated … More cell death. These results show the delayed neuronal loss in the distant, non-ischemic areas after focal cerebral ischemia. These neuropatholocgical changes in the ipsilateral thalamus and substantia nigra initially found in the rat MCA occlusion model similarly occurred in clinical cases of cerebral infraction in the MCA territory. Secondary, we examined the effect of MK-801 on focal cerebral ischemia model. Consequently, the area of infraction in the cerebral cortex was significantly decreased in the treated group. The results show that the excitotoxic mechanism may be responsible for ischemic injury in the cortical neurons. Thirdly, we studied behavioral changes after focal cerebral ischemia in rats. The MCA-occluded animals showed a significant impairment of learning behavior compared to the sham-operated animals in the one trial passive avoidance response and also active avoidance response. In the active avoidance task, the the learning impairment closely correlated with tissue damage, although the correlation was not observed in the passive avoidance task. Less