Kemppainen S, Pitkänen A
Epilepsy Research Laboratory, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, PO Box 1627, FIN-70211 Kuopio, Finland.
Neuroscience. 2004;126(2):485-501. doi: 10.1016/j.neuroscience.2004.03.015.
Both the amygdala and hippocampus are damaged in drug-resistant temporal lobe epilepsy (TLE), suggesting that amygdalo-hippocampal interconnectivity is compromised in TLE. Therefore, we examined one of the major projections from the amygdala to the hippocampus, the projection from the amygdala to the CA1 subfield of the hippocampus/subiculum border region, and assessed whether it is preserved in rats with spontaneous seizures. Male Wistar rats were injected with kainic acid (9 mg/kg, i.p.) to induce chronic epilepsy. The occurrence of spontaneous seizures was monitored 5 or 15 weeks later by video-recording the rats for up to 5 days. Saline-injected animals served as controls. Thereafter, the retrograde tracer Fluoro-gold was injected into the border region of the temporal CA1/subiculum. Rats were perfused for histology 1-2 weeks later and sections were immunohistochemically processed to detect Fluoro-gold-positive cells. Comparison of the labeling in control and epileptic tissue indicated that a large cluster of retrogradely labeled cells in the parvicellular division of the basal nucleus was well preserved in epilepsy, even when the neuronal damage in the amygdala was substantial. Another large cluster of retrogradely labeled cells in the lateral division of the amygdalo-hippocampal area, the posterior cortical nucleus (part of the vomeronasal amygdala), and the periamygdaloid cortex (part of the olfactory amygdala), however, had disappeared in epileptic brain in parallel to severe neuronal loss in these nuclei. These data demonstrate that a projection from the parvicellular division of the basal nucleus to the temporal CA1/subiculum region is resistant to status epilepticus-induced neuronal damage and provides a candidate pathway by which seizure activity can spread and propagate from the amygdala to the hippocampal formation.
杏仁核和海马体在耐药性颞叶癫痫（TLE）中均受到损伤，这表明杏仁核 - 海马体之间的相互连接性在TLE中受到损害。因此，我们研究了从杏仁核到海马体的主要投射之一，即从杏仁核到海马体/下托边界区域的CA1亚区的投射，并评估其在自发性癫痫发作的大鼠中是否得以保留。雄性Wistar大鼠腹腔注射海藻酸（9 mg/kg）以诱导慢性癫痫。5周或15周后，通过对大鼠进行长达5天的视频记录来监测自发性癫痫发作的发生情况。注射生理盐水的动物作为对照。此后，将逆行示踪剂荧光金注射到颞叶CA1/下托的边界区域。1 - 2周后对大鼠进行灌注以进行组织学检查，并对切片进行免疫组织化学处理以检测荧光金阳性细胞。对照组织和癫痫组织中标记的比较表明，即使杏仁核中的神经元损伤严重，基底核小细胞部中一大簇逆行标记细胞在癫痫状态下仍保存完好。然而，杏仁核 - 海马区外侧部、后皮质核（犁鼻杏仁核的一部分）和杏仁周皮质（嗅觉杏仁核的一部分）中的另一大簇逆行标记细胞在癫痫脑中已消失，同时这些核中出现了严重的神经元丢失。这些数据表明，从基底核小细胞部到颞叶CA1/下托区域的投射对癫痫持续状态诱导的神经元损伤具有抗性，并提供了一条癫痫活动可以从杏仁核传播到海马结构的候选途径。
