Tremblay E, Ben-Ari Y
Rev Electroencephalogr Neurophysiol Clin. 1984 Dec;14(3):241-6. doi: 10.1016/s0370-4475(84)80011-8.
Systemic injections of kainic acid (KA) in adult rats rapidly induce sustained motor seizures preferentially involving the limbic structures and culminating in status epilepticus. The hippocampal formation and amygdala seem to occupy a central position for the onset of paroxysmal discharge and for the manifestation of limbic signs respectively. With long survival periods, the animals spontaneously display limbic motor seizures and a second administration of KA produces more severe effects. The brain damage, found in several limbic structures subsequent to KA-induced seizures, is reminiscent of that seen in human epileptics, and electrographical and metabolic studies (using the 2-deoxyglucose method) reveal that it follows increased neuronal and metabolic activation. The crucial role of the mossy fiber system in the particular vulnerability to KA of the CA3 neurons of Ammon's horn is also suggested by a study of the maturation of the KA-induced seizure and brain damage syndrome.
给成年大鼠全身注射海藻酸（KA）会迅速引发持续的运动性癫痫发作，优先累及边缘结构，最终导致癫痫持续状态。海马结构和杏仁核似乎分别在阵发性放电的起始和边缘体征的表现中占据中心位置。在较长的存活期内，动物会自发出现边缘性运动性癫痫发作，再次注射KA会产生更严重的影响。KA诱导的癫痫发作后，在几个边缘结构中发现的脑损伤让人联想到人类癫痫患者的脑损伤，并且电生理学和代谢研究（使用2-脱氧葡萄糖法）表明，这是神经元和代谢激活增加之后出现的结果。对KA诱导的癫痫发作和脑损伤综合征成熟过程的一项研究也表明，苔藓纤维系统在海马角CA3神经元对KA的特殊易损性中起关键作用。
