Wiemann M, Altrup U, Speckmann E J
Institut für Experimentelle Epilepsieforschung, Münster, Germany.
Neurosci Lett. 1997 Nov 21;237(2-3):101-4. doi: 10.1016/s0304-3940(97)00818-5.
Spread of epileptic activity was studied by inducing epileptiform activity (pentylenetetrazol, PTZ) in one part of a nervous system and by analyzing responses of neurons in a non-PTZ-treated part (identified neurons, paired buccal ganglia, Helix pomatia). Paroxysmal depolarization shifts (PDS) induced time-locked depolarizations in non-epileptic neurons (latency ca. 5 s, duration ca. 1 min, amplitude < or =20 mV). Amplitudes were augmenting during several hours of epileptic activity. Depolarizations were accompanied by an increase in membrane resistance and they were blocked in 'high Mg-low Ca' solutions. It is assumed that the potentials represent a typical widespread response of non-epileptic neurons to PDS of other neurons. This response may be induced via non-specific releases of substances of the epileptically active neurons thereby activating neighboring neurons which in turn activate neurons in control ganglion.
通过在神经系统的一部分诱导癫痫样活动（戊四氮，PTZ）并分析未用PTZ处理部分（已识别神经元、成对颊神经节、苹果螺）中神经元的反应，研究癫痫活动的传播。阵发性去极化偏移（PDS）在非癫痫神经元中诱导出时间锁定的去极化（潜伏期约5秒，持续时间约1分钟，幅度≤20 mV）。在癫痫活动的几个小时内，幅度不断增大。去极化伴随着膜电阻的增加，并且在“高镁低钙”溶液中被阻断。据推测，这些电位代表非癫痫神经元对其他神经元PDS的典型广泛反应。这种反应可能通过癫痫活动神经元物质的非特异性释放来诱导，从而激活相邻神经元，而相邻神经元又激活控制神经节中的神经元。
