PDF(Pubmed)
Abstract：
Granule cell dispersion (GCD) has been associated as a pathological feature of temporal lobe epilepsy (TLE). Early-life epileptiform activity such as febrile seizures has been proposed to have a causal link to developing chronic TLE. During postnatal development, the hippocampus may be particularly vulnerable to hyperexcitability-induced insults since neuronal migration and differentiation are still ongoing in the hippocampus. Further, the extracellular matrix (ECM), here in particular the protein reelin, has been implicated in the pathophysiology of GCD. Thus, loss of reelin-expressing cells, Cajal-Retzius cells and subsets of interneurons, may be related to GCD. To study the possible role of febrile seizures, we previously induced GCD in vitro by subjecting hippocampal slice cultures to a transient heat-shock, which was not accompanied by loss of Cajal-Retzius cells. In order to examine the mechanisms involved in heat-shock induced GCD, the present study aimed to determine whether such dispersion could be prevented by blocking cellular electrical activity. Here we show that the extent of heat-shock induced GCD could be significantly reduced by treatment with the sodium channel blocker tetrodotoxin (TTX), suggesting that electrical activity is an important factor involved in heat-shock induced GCD.
摘要：
颗粒细胞分散（GCD）已被视为颞叶癫痫（TLE）的病理特征。有人提出，诸如高热惊厥之类的早期癫痫样活动与发展为慢性TLE有因果关系。在产后发育过程中，海马区可能特别容易受到兴奋过度诱导的损伤,因为海马区的神经元迁移和分化仍在进行.Further,细胞外基质（ECM），这里特别是reelin蛋白，与GCD的病理生理学有关。因此，reelin表达细胞的损失，Cajal-Retzius细胞和中间神经元亚群，可能与GCD有关。为了研究高热惊厥的可能作用，我们先前通过对海马切片培养物进行短暂的热休克体外诱导GCD，不伴有Cajal-Retzius细胞的损失。为了研究热休克诱导的GCD的机制，本研究旨在确定这种分散是否可以通过阻断细胞电活动来预防。在这里，我们表明，热休克诱导的GCD的程度可以通过钠通道阻滞剂河豚毒素（TTX）治疗显着降低，表明电活动是热休克诱导的GCD的重要因素。
