Sater R A, Nadler J V
Department of Pharmacology, Duke University Medical Center, Durham, NC 27710.
Neurosci Lett. 1988 Jan 11;84(1):73-8. doi: 10.1016/0304-3940(88)90340-0.
To analyze the relation between kainic acid-induced limbic seizures and the associated brain lesions, various doses of kainic acid (117-940 pmol) were administered intracerebroventricularly to unanesthetized rats. Rats which experienced status epilepticus developed lesions in several limbic, neocortical and thalamic regions. However, rats which experienced only temporally discrete seizures (less than 30 min each) suffered neuronal degeneration exclusively in the CA3-CA4 area ipsilateral to the kainic acid infusion, even when other regions exhibited the same total electrographic seizure duration. These results can best be explained by postulating that, in addition to evoking seizures, kainic acid also enhances the toxic effects of seizures on CA3-CA4 neurons.
为分析海藻酸诱导的边缘叶癫痫发作与相关脑损伤之间的关系，将不同剂量的海藻酸（117 - 940皮摩尔）经脑室内注射给未麻醉的大鼠。经历癫痫持续状态的大鼠在几个边缘叶、新皮质和丘脑区域出现损伤。然而，仅经历短暂性离散发作（每次发作少于30分钟）的大鼠，即使其他区域表现出相同的总脑电图癫痫发作持续时间，也仅在海藻酸注入同侧的CA3 - CA4区域出现神经元变性。这些结果最好通过假设来解释，即除了诱发癫痫发作外，海藻酸还增强了癫痫发作对CA3 - CA4神经元的毒性作用。
