Kelley M S, Steward O
Department of Neuroscience, University of Virginia, Charlottesville 22908, USA.
Exp Neurol. 1996 May;139(1):73-82. doi: 10.1006/exnr.1996.0082.
Destruction of the entorhinal cortex (EC) triggers a number of cellular and molecular responses in the denervated hippocampus and dentate gyrus. The signals that trigger these changes are not known but could include physiological events that occur during the production of the injury or during the early postlesion period. Of particular interest is whether experimental lesions induce seizures and/or spreading depression (SD), both of which have been shown to dramatically alter neuronal and glial gene expression. In the present study, acute neurophysiological techniques were used to evaluate whether seizures or SD occur during the production of EC lesions. Chronic recording techniques were used to monitor electroencephalographic (EEG) activity during the first 24 h after the injury in order to evaluate the extent of postlesion seizures. One or more episodes of SD occurred in 9 of 13 animals during the production of electrolytic EC lesions. However, hippocampal seizures were not observed except for very brief episodes of seizure activity at the onset of an episode of SD. Chronic recordings of postlesion EEG activity revealed that spontaneous electrographic seizures occurred during the first 24 h postlesion in all animals. The spontaneous electrographic seizures were approximately 30 s in duration and were not accompanied by motor convulsions. The first seizures occurred within several hours after the lesion, and seizures continued to occur periodically (at an average frequency of 0.42 per hour) over the 24-h recording period. Seizures occurred on the side of the brain ipsilateral to the lesion in all animals and occurred on the side contralateral to the lesion in 3 of 5 animals. These results indicate that EC lesions produce physiological events that occur variably in different animals; these processes may account for some of the variability in the cellular responses to this "standardized" injury.
内嗅皮层(EC)的破坏会在去神经支配的海马体和齿状回中引发一系列细胞和分子反应。触发这些变化的信号尚不清楚,但可能包括损伤产生过程中或损伤后早期发生的生理事件。特别令人感兴趣的是,实验性损伤是否会诱发癫痫发作和/或扩散性抑制(SD),这两者均已被证明会显著改变神经元和胶质细胞的基因表达。在本研究中,采用急性神经生理学技术来评估在制作EC损伤时是否会发生癫痫发作或SD。使用慢性记录技术来监测损伤后最初24小时内的脑电图(EEG)活动,以评估损伤后癫痫发作的程度。在制作电解性EC损伤的过程中,13只动物中有9只出现了一次或多次SD发作。然而,除了在SD发作开始时出现的非常短暂的癫痫活动外,未观察到海马体癫痫发作。损伤后EEG活动的慢性记录显示,所有动物在损伤后最初24小时内均出现了自发性脑电图癫痫发作。自发性脑电图癫痫发作持续时间约为30秒,且不伴有运动性惊厥。首次癫痫发作发生在损伤后的数小时内,并且在24小时的记录期内癫痫发作持续周期性出现(平均频率为每小时0.42次)。所有动物的癫痫发作均发生在损伤同侧的大脑半球,5只动物中有3只在损伤对侧的大脑半球也出现了癫痫发作。这些结果表明,EC损伤会产生在不同动物中变化不定的生理事件;这些过程可能解释了对这种“标准化”损伤的细胞反应中的一些变异性。