Sawamura Atsushi, Hashizume Kiyotaka, Tanaka Tatsuya
Department of Neurosurgery, Asahikawa Medical College, 2-1, Midorigaoka-Higashi, 078-8510 Asahikawa, Japan.
Brain Res. 2002 May 10;935(1-2):1-8. doi: 10.1016/s0006-8993(02)02231-x.
There has been few studies of the globus pallidus in relation to epilepsy. In this study, kainic acid (KA)-induced globus pallidus seizure was electrophysiologically, electroencephalographically, histopathologically and metabolically investigated in rats. Sixteen Wistar rats weighing 250-350 g were used. Under intraperitoneal pentobarbital anesthesia, a stainless-steel cannula was inserted stereotaxically into the left globus pallidus pars externa (GPe) for KA injection. For recording EEG, a depth electrode was inserted into the left GPe, just posterior to the tip of the injection guide cannula. Electrodes were also inserted into the right globus pallidus and bilateral sensorimotor cortex (SMC). EEG changes after KA injection were classified as follows: Continuous low-voltage spikes were observed in the left GPe on EEG at stage 1. Intermittent multiple spikes and wave complexes began to propagate to the left SMC at stage 2. Continuous spikes and wave complexes began to propagate to the bilateral SMC at stage 3. Secondary generalized seizures were observed at stage 4. Globus pallidus seizures recurred every 7-9 min and lasted for 4-6 h. However, the seizures gradually subsided and became normal within 18 h. No spontaneous seizure was detected for the next 30 days. Histopathological study revealed a small gliotic lesion with neuronal cell loss around the cannula tip. Neither degeneration nor neuronal cell loss in the ipsilateral hippocampus were observed. The autoradiogram using [14C]2-deoxyglucose during seizure status demonstrated a remarkable increase of local cerebral glucose utilization not only in the GPe but also in the GPi. An increase glucose metabolism was also found in the follows: the medial and lateral septal nucleus, substantia nigra, hippocampus, frontal cortex, parietal cortex, piriform cortex, entorhinal cortex, accumbens nucleus, ventral and lateral nucleus of the thalamus, amygdala, and ventral nucleus of hypothalamus. KA injection into the unilateral GPe evoked not only epileptic excitation of the cortex but also transient enhancement of the globus pallidus-substantia nigra circuit.
关于苍白球与癫痫关系的研究较少。在本研究中,对大鼠进行了电生理学、脑电图学、组织病理学和代谢方面的研究,以观察海人酸(KA)诱导的苍白球癫痫发作情况。选用16只体重250 - 350 g的Wistar大鼠。在腹腔注射戊巴比妥麻醉下,通过立体定向将不锈钢套管插入左侧苍白球外侧部(GPe)用于注射KA。为记录脑电图,在注射引导套管尖端后方将深度电极插入左侧GPe。电极还插入右侧苍白球和双侧感觉运动皮层(SMC)。KA注射后的脑电图变化分类如下:第1阶段脑电图显示左侧GPe出现持续的低电压棘波。第2阶段间歇性多棘波和波复合波开始向左侧SMC传播。第3阶段持续的棘波和波复合波开始向双侧SMC传播。第4阶段观察到继发性全身性癫痫发作。苍白球癫痫发作每7 - 9分钟复发一次,持续4 - 6小时。然而,癫痫发作逐渐缓解并在18小时内恢复正常。在接下来的30天内未检测到自发性癫痫发作。组织病理学研究显示套管尖端周围有小的胶质增生病变伴神经元细胞丢失。同侧海马未观察到变性或神经元细胞丢失。在癫痫发作状态下使用[14C]2 - 脱氧葡萄糖的放射自显影片显示,不仅GPe而且苍白球内侧部(GPi)的局部脑葡萄糖利用显著增加。在以下区域也发现葡萄糖代谢增加:内侧和外侧隔核、黑质、海马、额叶皮层、顶叶皮层、梨状皮层、内嗅皮层、伏隔核、丘脑腹侧和外侧核、杏仁核以及下丘脑腹侧核。向单侧GPe注射KA不仅诱发皮层的癫痫性兴奋,还引起苍白球 - 黑质回路的短暂增强。