Rocha L, Kaufman D L
Instituto Mexicano de Psiquiatría, Mexico City, Mexico.
Neurosci Lett. 1998 Jan 30;241(2-3):111-4. doi: 10.1016/s0304-3940(98)00002-0.
Repeated subconvulsive electrical stimulation of the amygdala leads to generalized seizures and provides an experimental model of epileptogenesis. Following electrical kindling stimulation the expression of c-Fos is rapidly induced. To evaluate the role of FOS protein in epileptogenesis, we used an antisense oligonucleotide strategy designed to inhibit its expression in the brain. Experimental and control oligonucleotides were delivered directly into the amygdala just prior to electrical stimulation. Immunocytochemical analysis showed that the administration of c-Fos antisense (but not sense) oligonucleotides inhibited expression of FOS in the amygdala following electrical stimulation. Behaviorally, treatment with c-Fos antisense oligonucleotides significantly accelerated the development of fully kindled (stage V) seizures. These data suggest that the increased FOS expression following electrical stimulation may be part of a protective mechanism which acts to inhibit epileptogenesis in the amygdala.
对杏仁核进行反复的亚惊厥性电刺激会导致全身性癫痫发作，并提供了一个癫痫发生的实验模型。在电点燃刺激后，c-Fos的表达会迅速被诱导。为了评估FOS蛋白在癫痫发生中的作用，我们采用了一种反义寡核苷酸策略，旨在抑制其在大脑中的表达。在电刺激之前，将实验性和对照性寡核苷酸直接注入杏仁核。免疫细胞化学分析表明，给予c-Fos反义（而非正义）寡核苷酸可抑制电刺激后杏仁核中FOS的表达。在行为学上，用c-Fos反义寡核苷酸治疗可显著加速完全点燃（V期）癫痫发作的发展。这些数据表明，电刺激后FOS表达的增加可能是一种保护机制的一部分，该机制可抑制杏仁核中的癫痫发生。
