Shoji Y, Tanaka E, Yamamoto S, Maeda H, Higashi H
Department of Physiology, Kurume University School of Medicine, Kurume 830, Japan.
J Neurophysiol. 1998 Aug;80(2):638-46. doi: 10.1152/jn.1998.80.2.638.
To elucidate the mechanism underlying epileptiform discharges in kindled rats, synaptic responses in kindled basolateral amygdala neurons in vitro were compared with those from control rats by using intracellular and whole cell patch-clamp recordings. In kindled neurons, electrical stimulation of the stria terminalis induced epileptiform discharges. The resting potential, apparent input resistance, current-voltage relationship of the membrane, and the threshold, amplitude, and duration of action potentials in kindled neurons were not different from those in control neurons. The electrical stimulation of stria terminalis elicited excitatory postsynaptic potentials (EPSPs) and DL-2-amino-5-phosphonopentanoic acid (AP5)-sensitive and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive excitatory postsynaptic currents (EPSCs). The amplitude of evoked EPSPs and of evoked AP5-sensitive and CNQX-sensitive EPSCs were enhanced markedly, whereas fast and slow inhibitory postsynaptic potentials (IPSPs) induced by electrical stimulation of lateral amygdaloid nucleus were not significantly different. The rise time and the decay time constant of the evoked CNQX-sensitive EPSCs were shortened, whereas the rise time of the evoked AP5-sensitive EPSCs was shortened, but the decay time constants were not significantly different. In both tetrodotoxin (TTX)-containing medium and low Ca2+ and TTX-containing medium, the frequency and amplitude of spontaneous EPSCs were increased in kindled neurons. These increases are presumably due to nearly synchronous multiquantal events resulted from the increased probability of Glu release at the nerve terminals. The rise time of evoked CNQX- and AP5-sensitive EPSCs and the decay time constant of evoked CNQX-sensitive EPSCs were shortened, suggesting that excitatory synapses at the proximal dendrite and/or the soma in kindled neurons may contribute more effectively to generate evoked EPSCs than those at distal dendrites. In conclusion, the increases in the amplitudes of spontaneous and evoked EPSCs and in the frequency of spontaneous EPSCs may contribute to the epileptiform discharges in kindled neurons.
为阐明点燃大鼠癫痫样放电的潜在机制，通过细胞内和全细胞膜片钳记录，比较了点燃大鼠基底外侧杏仁核神经元与对照大鼠神经元的突触反应。在点燃的神经元中，终纹床核的电刺激可诱发癫痫样放电。点燃神经元的静息电位、表观输入电阻、膜的电流-电压关系以及动作电位的阈值、幅度和持续时间与对照神经元并无差异。终纹床核的电刺激可引发兴奋性突触后电位（EPSP）以及对DL-2-氨基-5-膦酰基戊酸（AP5）敏感和对6-氰基-7-硝基喹喔啉-2,3-二酮（CNQX）敏感的兴奋性突触后电流（EPSC）。诱发的EPSP幅度以及诱发的对AP5敏感和对CNQX敏感的EPSC幅度均显著增强，而杏仁核外侧核电刺激诱发的快速和慢速抑制性突触后电位（IPSP）并无显著差异。诱发的对CNQX敏感的EPSC的上升时间和衰减时间常数缩短，而诱发的对AP5敏感的EPSC的上升时间缩短，但衰减时间常数并无显著差异。在含河豚毒素（TTX）的培养基以及低钙和含TTX的培养基中，点燃神经元的自发性EPSC频率和幅度均增加。这些增加可能是由于神经末梢谷氨酸释放概率增加导致的近乎同步的多量子事件所致。诱发的对CNQX和对AP5敏感的EPSC的上升时间以及诱发的对CNQX敏感的EPSC的衰减时间常数缩短，表明点燃神经元近端树突和/或胞体处的兴奋性突触可能比远端树突处的突触更有效地促成诱发EPSC的产生。总之，自发性和诱发EPSC幅度的增加以及自发性EPSC频率的增加可能促成了点燃神经元的癫痫样放电。
