Jyoti Amar, Sethi Pallavi, Sharma Deepak
Neurobiology Laboratory, School of Life Sciences, Jawaharlal Nehru University, New Delhi, India.
Neurosci Lett. 2009 Apr 3;453(2):86-91. doi: 10.1016/j.neulet.2009.01.082. Epub 2009 Feb 7.
Traumatic brain injury is a major risk of post-traumatic epilepsy in a large number of individuals of different age groups. Lots of research has been done to elucidate the mechanism of post-traumatic epileptogenesis but age-related vulnerability to develop traumatic seizures is still unknown. Therefore, in the present study investigations were carried out to characterize the electrobehavioral seizure manifestation and associated alterations in young and old epileptic groups. FeCl(3) injection model was used to induce post-traumatic seizures as this model closely resembles human post-traumatic epilepsy. Synchronized video-EEG monitoring was performed to diagnose manifestation of seizures in young (4 months) and old (18 months) rats. Biochemical and ultrastructural studies were performed to determine the mechanism behind the altered age-related vulnerability for post-traumatic seizures. Our result shows that old rats were more vulnerable to post-traumatic epilepsy due to faster seizure spread and lower latency for generalization of electro-clinical seizure activity. The observed biochemical and microscopic alterations associated with old age positively correlate with the altered susceptibility to develop seizures in old epileptic groups.
创伤性脑损伤是不同年龄组大量个体发生创伤后癫痫的主要风险因素。为阐明创伤后癫痫发生的机制已开展了大量研究,但年龄相关的创伤性癫痫发作易感性仍不清楚。因此,在本研究中,我们进行了调查,以描述年轻和老年癫痫组的电行为性癫痫发作表现及相关改变。采用氯化铁注射模型诱导创伤后癫痫发作,因为该模型与人类创伤后癫痫非常相似。对年轻(4个月)和老年(18个月)大鼠进行同步视频脑电图监测,以诊断癫痫发作表现。进行生化和超微结构研究,以确定与年龄相关的创伤后癫痫发作易感性改变背后的机制。我们的结果表明,老年大鼠因癫痫发作传播更快和电临床癫痫活动泛化潜伏期更短而更容易发生创伤后癫痫。在老年癫痫组中观察到的与衰老相关的生化和微观改变与癫痫发作易感性改变呈正相关。