Uva Laura, Saccucci Stefania, Chikhladze Maia, Tassi Laura, Gnatkovsky Vadym, Milesi Gloria, Morbin Michela, de Curtis Marco
Unit of Epileptology.
Unit of Neuropathology, and.
J Neurosci. 2017 Mar 29;37(13):3544-3554. doi: 10.1523/JNEUROSCI.2239-16.2016. Epub 2017 Mar 6.
Seizure patterns identified in focal epilepsies caused by diverse etiologies are likely due to different pathogenic mechanisms. We describe here a novel, region-specific focal seizure pattern that mimics seizure activity observed in a subpopulation of patients submitted to presurgical monitoring with intracerebral electrodes. Distinctive seizure-like events (SLEs) are induced in the olfactory regions by acute treatment of both tangential brain slices and the isolated guinea pig brain with the potassium channel blocker 4-aminopyridine. Analysis of field potentials, intracellular activities, and extracellular potassium changes demonstrates that SLEs in the piriform cortex initiate in the superficial layer 1 lacking principal neurons with an activity-dependent increase of extracellular potassium. SLE progression (but not onset) does not require the participation of synaptic transmission and is mediated by diffusion of potassium to deep cortical layers. The novel seizure pattern here described is not observed in other cortical regions; it is proposed to rely on the peculiar organization of the superficial piriform cortex layers, which are characterized by unmyelinated axons and perisynaptic astroglial envelopes. This study reveals a sequence of ictogenic events in the olfactory cortex that were never described before in other cortical structures and supports the notion that altered potassium homeostasis and unmyelinated fibers may represent a potential vehicle for focal ictogenesis. We describe a novel seizure pattern peculiar of the olfactory cortex that resembles focal seizures with low-voltage fast activity at onset observed in humans. The findings suggest that network mechanisms responsible for seizure onset can be region specific.
由多种病因引起的局灶性癫痫中所识别出的癫痫发作模式，可能归因于不同的致病机制。我们在此描述一种新的、区域特异性的局灶性癫痫发作模式，它类似于在接受脑内电极术前监测的部分患者中观察到的癫痫发作活动。通过用钾通道阻滞剂4-氨基吡啶对切线脑片和分离的豚鼠脑进行急性处理，可在嗅觉区域诱发独特的癫痫样事件（SLEs）。场电位、细胞内活动和细胞外钾变化的分析表明，梨状皮质中的SLEs起始于缺乏主要神经元的浅层1，细胞外钾随着活动依赖性增加。SLE的进展（但不是起始）不需要突触传递的参与，而是由钾扩散到皮质深层介导的。此处描述的这种新的癫痫发作模式在其他皮质区域未观察到；它被认为依赖于浅层梨状皮质层的特殊组织结构，其特征是无髓鞘轴突和突触周围星形胶质细胞包膜。这项研究揭示了嗅觉皮质中一系列以前在其他皮质结构中从未描述过的致痫事件，并支持了钾稳态改变和无髓鞘纤维可能代表局灶性癫痫发生的潜在载体这一观点。我们描述了一种嗅觉皮质特有的新癫痫发作模式，类似于在人类中观察到的起始时具有低电压快速活动的局灶性癫痫发作。这些发现表明，负责癫痫发作起始的网络机制可能具有区域特异性。
