Ylinen A, Lahtinen H, Sirviö J, Partanen J, Asikainen A, Gulyas A, Freund T F, Riekkinen P
Department of Neurology, University of Kuopio, Finland.
Brain Res. 1991 Jul 12;553(2):195-200. doi: 10.1016/0006-8993(91)90824-f.
Sustained stimulation of the perforant path has been shown to damage the CA1 area and impair spatial memory in rats. The pattern of cell death is similar in human epileptics, who also exhibit memory deficits. In this study we demonstrate that the learning/memory impairment in water maze test and the development of interictal spikes that also followed stimulation-induced damage were antagonized by CGP 39551. Pretreatment with this NMDA receptor antagonist also slightly diminished somatostatin cell loss in the hilus but not CA1 pyramidal cell damage. These results indicate that the impairment of spatial learning/memory seems to be dependent not only on the degree of cell degeneration in the CA1 subfield of the hippocampus but also on the frequency of interictal spikes, at least in this model of epilepsy.
持续刺激穿通通路已被证明会损害大鼠的CA1区并损害其空间记忆。人类癫痫患者的细胞死亡模式与之相似，他们也表现出记忆缺陷。在本研究中，我们证明，CGP 39551可拮抗水迷宫试验中的学习/记忆损伤以及刺激诱导损伤后出现的发作间期棘波的产生。用这种NMDA受体拮抗剂预处理也可略微减少海马门区生长抑素细胞的丢失，但对CA1锥体细胞损伤无影响。这些结果表明，空间学习/记忆的损伤似乎不仅取决于海马CA1亚区细胞变性的程度，还取决于发作间期棘波的频率，至少在这种癫痫模型中是如此。
