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首页> 外文期刊>The European Journal of Neuroscience >Long-lasting modification of intrinsic discharge properties in subicular neurons following status epilepticus.
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Long-lasting modification of intrinsic discharge properties in subicular neurons following status epilepticus.

机译：癫痫持续状态后，特定神经元内在放电特性的持久修饰。

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A single episode of status epilepticus (SE) induces neuropathological changes in the brain that may lead to the development of a permanent epileptic condition. Most studies of this plasticity have focused on the hippocampus, where both synaptic function and intrinsic neuronal excitability have been shown to be persistently modified by SE. However, many other brain structures are activated during SE and may also be involved in the subsequent epileptogenic process. Here we have investigated whether SE, induced in rats with pilocarpine and terminated after 40 min with diazepam, persistently modifies the intrinsic excitability of pyramidal neurons in the subiculum. Subicular slices were prepared from control and SE-experienced rats (2-5 weeks after SE). In the control group, only 4% of the neurons fired bursts in response to intrasomatic, threshold-straddling depolarizing current pulses (low-threshold bursters). The remaining neurons either fired bursts in response to strong (3x threshold) depolarizations (35%; high-threshold bursters) or fired in a completely regular mode (61%; nonbursters). In the SE-experienced group, the fractions of low- and high-threshold bursters markedly increased to 29% and 53%, respectively. This change in firing behaviour was associated with a marked increase in the size of the spike afterdepolarization, particularly in low-threshold bursters. Experimental suppression of Ca2+ currents selectively blocked low-threshold bursting but did not affect high-threshold bursting, suggesting that a dual Ca2+- dependent and Ca2+- independent mechanism controls bursting in these neurons. The persistent up-regulation of intrinsic bursting in the subiculum, in concert with similar changes in the hippocampus, undoubtedly contributes to epileptogenesis following pilocarpine-induced SE.
机译：癫痫持续状态（SE）的单一发作会诱发大脑中的神经病理变化，这可能导致永久性癫痫病的发展。关于这种可塑性的大多数研究都集中在海马上，其中海马突触功能和内在神经元兴奋性均已被SE持续修饰。然而，许多其他的大脑结构在SE期间被激活，也可能参与随后的癫痫发生过程。在这里，我们研究了在毛果芸香碱大鼠中诱发并在地西m 40分钟后终止的SE是否会持续改变下丘脑锥体神经元的内在兴奋性。从对照和有SE经历的大鼠（SE后2-5周）制备亚块状切片。在对照组中，只有4％的神经元响应体细胞内跨阈值的去极化电流脉冲而触发突发（低阈值突发信号）。其余的神经元要么响应强去极化（3x阈值;高阈值突发脉冲）而触发爆发（以完全规律的模式触发）（61％;非突发）。在有SE经验的组中，低阈值和高阈值突发事件的比例分别显着增加到29％和53％。发射行为的这种变化与去极化后尖峰的大小显着增加有关，特别是在低阈值突发脉冲中。对Ca2 +电流的实验抑制选择性地阻止了低阈值爆发，但不影响高阈值爆发，这表明依赖于Ca2 +和Ca2 +的双重机制控制了这些神经元的爆发。持续的上皮下突突的持续上调，与海马体的类似变化一致，无疑会导致毛果芸香碱诱发的SE后癫痫发生。

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