Cellular and network properties of the subiculum in the pilocarpine model of temporal lobe epilepsy
Cellular and network properties of the subiculum in the pilocarpine model of temporal lobe epilepsy
复制标题
DOI：
10.1002/cne.20460
复制
发表时间：
2005-03-21
影响因子：
2.5
通讯作者：
Behr, J
中科院分区：
文献类型：
--
作者：
Knopp, A;Kivi, A;Behr, J
近来研究表明，枕下在人类颞叶癫痫的间歇活动的产生中起着至关重要的作用。使用匹罗卡品癫痫模型，本研究探讨了记录在耻骨下的网络高兴奋性的解剖学基础。用荧光染料染色和重建常规和突发尖峰的丘下锥体细胞，以分析癫痫引起的树突和轴突系统的改变。在对照动物中，突发尖峰细胞的数量约为正常尖峰细胞的2比1。规则型和突发性尖峰细胞具有广泛的轴突分支和auttap样接触，表明它们具有高度的内在连通性。此外，向CA1突出的丘下轴突表明存在CA1-丘下-CA1回路。在服用匹罗卡品的大鼠的丘下，我们发现网络兴奋性增强，其特征是自发节律活动、多突触反应和全或无诱发的动作电位爆发。匹罗卡品处理大鼠的骨下细胞损失约30%。与对照制剂相比，规则型和突发型细胞的比例实际上是相反的。根尖树突近端部分的乔木化和脊柱密度降低提示CA1部分失分化。在匹罗卡品处理的大鼠中，未观察到锥体细胞轴突生长增加。因此，锥体下细胞的轴突发芽并不是病理事件发生的必要条件。我们认为，匹罗卡品诱发的癫痫发作会导致复发性丘下网络内突触接触的暴露或加强。(C) 2005 Wiley-Liss, Inc。
The subiculum was recently shown to be crucially involved in the generation of interictal activity in human temporal lobe epilepsy. Using the pilocarpine model of epilepsy, this study examines the anatomical substrates for network hyperexcitability recorded in the subiculum. Regular- and burst-spiking subicular pyramidal cells were stained with fluorescence dyes and reconstructed to analyze seizure-induced alterations of the dendritic and axonal system. In control animals burst-spiking cells outnumbered regular-spiking cells by about two to one. Regular- and burst-spiking cells were characterized by extensive axonal branching and autapse-like contacts, suggesting a high intrinsic connectivity. In addition, subicular axons projecting to CA1 indicate a CA1-subiculum-CA1 circuit. In the subiculum of pilocarpine-treated rats we found an enhanced network excitability characterized by spontaneous rhythmic activity, polysynaptic responses, and all-or-none evoked bursts of action potentials. In pilocarpine-treated rats the subiculum showed cell loss of about 30%. The ratio of regular- and burst-spiking cells was practically inverse as compared to control preparations. A reduced arborization and spine density in the proximal part of the apical dendrites suggests a partial deafferentiation from CA1. In pilocarpine-treated rats no increased axonal outgrowth of pyramidal cells was observed. Hence, axonal sprouting of subicular pyramidal cells is not mandatory for the development of the pathological events. We suggest that pilocarpine-induced seizures cause an unmasking or strengthening of synaptic contacts within the recurrent subicular network. (C) 2005 Wiley-Liss, Inc.