Polack Pierre-Olivier, Guillemain Isabelle, Hu Emilie, Deransart Colin, Depaulis Antoine, Charpier Stéphane
Institut National de la Santé et de la Recherche Médicale Unité 667, Collège de France, 75231 Paris, Cedex 05, France.
J Neurosci. 2007 Jun 13;27(24):6590-9. doi: 10.1523/JNEUROSCI.0753-07.2007.
Typical absence has long been considered as the prototypic form of generalized nonconvulsive epileptic seizures. Recent investigations in patients and animal models suggest that absence seizures could originate from restricted regions of the cerebral cortex. However, the cellular and local network processes of seizure initiation remain unknown. Here, we show that absence seizures in Genetic Absence Epilepsy Rats from Strasbourg, a well established genetic model of this disease, arise from the facial somatosensory cortex. Using in vivo intracellular recordings, we found that epileptic discharges are initiated in layer 5/6 neurons of this cortical region. These neurons, which show a distinctive hyperactivity associated with a membrane depolarization, lead the firing of distant cortical cells during the epileptic discharge. Consistent with their ictogenic properties, neurons from this "focus" exhibit interictal and preictal oscillations that are converted into epileptic pattern. These results confirm and extend the "focal hypothesis" of absence epilepsy and provide a cellular scenario for the initiation and generalization of absence seizures.
典型失神发作长期以来一直被视为全身性非惊厥性癫痫发作的原型形式。最近对患者和动物模型的研究表明，失神发作可能起源于大脑皮层的受限区域。然而，癫痫发作起始的细胞和局部网络过程仍然未知。在这里，我们表明，来自斯特拉斯堡的遗传性失神癫痫大鼠（一种该疾病成熟的遗传模型）的失神发作起源于面部躯体感觉皮层。通过体内细胞内记录，我们发现癫痫放电起始于该皮质区域的5/6层神经元。这些神经元表现出与膜去极化相关的独特过度活跃，在癫痫放电期间引发远处皮质细胞的放电。与其致痫特性一致，来自这个“病灶”的神经元表现出发作间期和发作前期振荡，这些振荡会转变为癫痫模式。这些结果证实并扩展了失神癫痫的“病灶假说”，并为失神发作的起始和扩散提供了细胞层面的情况。
