Ueda Y, Willmore L J, Triggs W J
Department of Neurology, University of Texas Medical School-Houston, Houston, Texas 77030, USA.
Exp Neurol. 1998 Sep;153(1):123-7. doi: 10.1006/exnr.1998.6869.
Rats were microinjected with a 100 mM aqueous solution of ferric chloride into the left amygdaloid body. Behavior was observed and depth electroencephalograms were recorded over the 30 days following injection. All of the FeCl3-injected rats developed isolated epileptiform discharges from the ipsilateral amygdala soon after injection. Within 5 days epileptiform discharges were arising as well from the contralateral amygdala and behavioral seizures were observed. These spontaneous seizures occurred in a pattern associated with stage 4 kindling, with rearing and bilateral forelimb clonus. Seizures persisted during the 30 days of the experiment. Recording from chronically implanted depth electrodes showed development of spike discharges, with recurrent seizures arising from amygdalar regions with propagation into both hippocampi. Aqueous iron is known to initiate lipid peroxidation by free radical mechanisms. Our observations suggest that epileptogenesis followed by chronic, spontaneous seizures could be initiated by deposition of iron-containing compounds into limbic structures of the rat.
将100 mM氯化铁水溶液微量注射到大鼠左侧杏仁核体中。在注射后的30天内观察行为并记录深度脑电图。所有注射FeCl3的大鼠在注射后不久同侧杏仁核就出现了孤立的癫痫样放电。5天内，对侧杏仁核也出现癫痫样放电，并观察到行为性癫痫发作。这些自发性癫痫发作的模式与4期点燃有关，表现为竖毛和双侧前肢阵挛。在实验的30天内癫痫发作持续存在。长期植入深度电极的记录显示出现了棘波放电，杏仁核区域反复出现癫痫发作并扩散到双侧海马体。已知水性铁通过自由基机制引发脂质过氧化。我们的观察结果表明，含铁化合物沉积到大鼠边缘结构中可能引发癫痫发生，随后出现慢性自发性癫痫发作。
