Mangan P S, Scott C A, Williamson J M, Bertram E H
Department of Neurology, University of Virginia Health Sciences Center, Charlottesville, VA 22908,USA.
Neuroscience. 2000;101(2):377-91. doi: 10.1016/s0306-4522(00)00358-4.
Limbic epilepsy is a chronic condition associated with a broad zone of seizure onset and pathology. Studies have focused mainly on the hippocampus, but there are indications that changes occur in other regions of the limbic system. This study used in vitro intracellular recording and histology to examine alterations to the physiology and anatomy of the basal nucleus of the amygdala in a rat model of chronic limbic epilepsy characterized by spontaneously recurring seizures. Epileptic pyramidal neuron responses evoked by stria terminalis stimulation revealed hyperexcitability characterized by multiple action potential bursts and no evident inhibitory potentials. In contrast, no hyperexcitability was observed in amygdalar neurons from kindled (included as a control for seizure activity) or control rats. Blockade of ionotropic glutamate receptors unmasked inhibitory postsynaptic potentials in epileptic pyramidal neurons. Control, kindled and epileptic inhibitory potentials were predominantly biphasic, with fast and slow components, but a few cells exhibited only the fast component (2/12 in controls, 0/3 in kindled, 3/10 in epileptic). Epileptic fast inhibitory potentials had a more rapid onset and shorter duration than control and kindled. Approximately 40% of control neurons exhibited spontaneous inhibitory potentials; no spontaneous inhibitory potentials were observed in neurons from kindled or epileptic rats. A preliminary histological examination revealed no gross alterations in the basal amygdala from epileptic animals. These results extend previous findings from this laboratory that hyperexcitability is found in multiple epileptic limbic regions and may be secondary to multiple alterations in excitatory and inhibitory efficacy. Because there were no differences between control and kindled animals, the changes observed in the epileptic animals are unlikely to be secondary to recurrent seizures.
边缘叶癫痫是一种与广泛的癫痫发作起始区和病理改变相关的慢性疾病。研究主要集中在海马体，但有迹象表明边缘系统的其他区域也发生了变化。本研究采用体外细胞内记录和组织学方法，在以自发性反复发作为特征的慢性边缘叶癫痫大鼠模型中，研究杏仁核基底核的生理和解剖学改变。终纹刺激诱发的癫痫性锥体神经元反应显示出过度兴奋性，其特征为多个动作电位爆发且无明显抑制电位。相比之下，在点燃大鼠（作为癫痫活动的对照）或对照大鼠的杏仁核神经元中未观察到过度兴奋性。离子型谷氨酸受体的阻断揭示了癫痫性锥体神经元中的抑制性突触后电位。对照、点燃和癫痫性抑制电位主要为双相，具有快速和慢速成分，但少数细胞仅表现出快速成分（对照组为2/12，点燃组为0/3，癫痫组为3/10）。癫痫性快速抑制电位的起始更快，持续时间比对照和点燃组更短。约40%的对照神经元表现出自发性抑制电位；在点燃或癫痫大鼠的神经元中未观察到自发性抑制电位。初步组织学检查显示癫痫动物的杏仁核基底核无明显改变。这些结果扩展了本实验室之前的发现，即在多个癫痫边缘叶区域发现了过度兴奋性，这可能继发于兴奋性和抑制性效能的多种改变。由于对照动物和点燃动物之间没有差异，癫痫动物中观察到的变化不太可能继发于反复癫痫发作。
