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Abstract：
Focal cortical dysplasia type I (FCD I) is the most common cause of pharmaco-resistant epilepsy with the poorest prognosis. To understand the epileptogenic mechanisms of FCD I, we obtained tissue resected from patients with FCD I epilepsy, and from tumor patients as control. Using whole-cell patch clamp in acute human brain slices, we investigated the cellular properties of fast-spiking interneurons (FSINs) and pyramidal neurons (PNs) within the ictal onset zone. In FCD I epilepsy, FSINs exhibited lower firing rates from slower repolarization and action potential broadening, while PNs had increased firing. Importantly, excitatory synaptic drive of FSINs increased progressively with the scale of cortical activation as a general property across species, but this relationship was inverted towards net inhibition in FCD I epilepsy. Further comparison with intracranial electroencephalography (iEEG) from the same patients revealed that the spatial extent of pathological high-frequency oscillations (pHFO) was associated with synaptic events at FSINs.
摘要：
局灶性皮质发育不良I型（FCDI）是耐药性癫痫的最常见原因，预后最差。为了了解FCDI的癫痫发生机制，我们获得了从FCDI癫痫患者切除的组织，肿瘤患者作为对照。在急性人脑切片中使用全细胞膜片钳，我们研究了发作区快速尖峰中间神经元（FSIN）和锥体神经元（PNs）的细胞特性。在FCDI型癫痫中，FSIN表现出较低的激发速率，来自较慢的复极化和动作电位展宽，而PN增加了射击。重要的是,FSIN的兴奋性突触驱动随着皮层激活的规模逐渐增加，作为跨物种的一般属性，但是这种关系在FCDI癫痫中被逆转为净抑制。与同一患者的颅内脑电图（iEEG）的进一步比较显示，病理性高频振荡（pHFO）的空间范围与FSIN的突触事件有关。
