Takebayashi Seiji, Hashizume Kiyotaka, Tanaka Tatsuya, Hodozuka Akira
Department of Neurosurgery, Asahikawa Medical College, Asahikawa, Japan.
Epilepsia. 2007 Feb;48(2):348-58. doi: 10.1111/j.1528-1167.2006.00948.x.
The present study aimed to clarify the effect of electrical stimulation and lesioning of the anterior nucleus of the thalamus (ANT) on kainic acid (KA)-induced focal cortical seizures in a rat model. To address the mechanism underlying these anticonvulsant actions, cerebral glucose metabolism after ANT electrical stimulation and lesioning was also examined.
Wistar rats were divided into five major groups: control (n = 9), unilateral (n = 9), and bilateral (n = 9) ANT electrical stimulation, and unilateral (n = 9) and bilateral (n = 9) ANT lesioning. After KA injection, average clinical-seizure frequencies in each group were measured. Electrical stimulation of ANT was introduced after induction of seizure status epilepticus. Stimulation was on for 30 min and off for 30 min per 60-min cycle. Local cerebral glucose utilization (LCGU) was also measured by using [(14)C] 2-deoxyglucose autoradiography in three groups of rats: control (n = 7), bilateral ANT stimulation (n = 7), and bilateral ANT lesioning (n = 7).
Unilateral ANT electrical stimulation and lesioning significantly reduced clinical seizure frequency, compared with control animals. Strikingly, no animals treated with bilateral ANT procedures demonstrated any clinical seizure. LCGU was markedly increased in the sensorimotor cortex, striatum, thalamus, mammillary body, and midbrain tegmentum of control group rats after KA injection, but no increase in LCGU was noted in rats treated with bilateral ANT lesioning or stimulation.
The electrical stimulation and lesioning of ANT suppressed focal cortical clinical seizures induced by KA injection. Additionally, an analysis of cerebral metabolic changes indicated that these procedures might suppress the function as amplifier and synchronizer of seizure activity.
本研究旨在阐明丘脑前核（ANT）电刺激和毁损对大鼠模型中 kainic 酸（KA）诱导的局灶性皮质癫痫发作的影响。为探讨这些抗惊厥作用的潜在机制，还检测了 ANT 电刺激和毁损后的脑葡萄糖代谢情况。
将 Wistar 大鼠分为五大组：对照组（n = 9）、单侧（n = 9）和双侧（n = 9）ANT 电刺激组，以及单侧（n = 9）和双侧（n = 9）ANT 毁损组。注射 KA 后，测量每组的平均临床癫痫发作频率。在癫痫持续状态诱导后进行 ANT 电刺激。每 60 分钟周期中，刺激持续 30 分钟，然后关闭 30 分钟。还使用[（14）C]2-脱氧葡萄糖放射自显影术，在三组大鼠中测量局部脑葡萄糖利用（LCGU）：对照组（n = 7）、双侧 ANT 刺激组（n = 7）和双侧 ANT 毁损组（n = 7）。
与对照动物相比，单侧 ANT 电刺激和毁损显著降低了临床癫痫发作频率。令人惊讶的是，接受双侧 ANT 操作的动物均未出现任何临床癫痫发作。KA 注射后，对照组大鼠的感觉运动皮层、纹状体、丘脑、乳头体和中脑被盖的 LCGU 显著增加，但双侧 ANT 毁损或刺激的大鼠未观察到 LCGU 增加。
ANT 的电刺激和毁损抑制了 KA 注射诱导的局灶性皮质临床癫痫发作。此外，对脑代谢变化的分析表明，这些操作可能抑制了癫痫活动的放大器和同步器功能。
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