Initiation of epileptiform activity in a rat model of periventricular nodular heterotopia.
Initiation of epileptiform activity in a rat model of periventricular nodular heterotopia.
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DOI：
10.1111/j.1528-1167.2011.03264.x
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发表时间：
2011-12
期刊：
影响因子：
5.6
通讯作者：
Schwartzkroin PA
中科院分区：
文献类型：
--
作者：
Tschuluun N;Jürgen Wenzel H;Doisy ET;Schwartzkroin PA
室周结节性异位（PNH），在人类中，往往与难以控制的癫痫。然而，关于PNH在癫痫发作产生和传播中的作用存在相当大的争议。为了研究这个问题，我们使用了一个大鼠模型，在该模型中，注射甲基偶氮甲醇（MAM）到怀孕的大鼠母鼠产生的后代与结节性异位样脑异常。电生理方法被用来检查活动的MAM诱导的PNH相对于活动在邻近的海马和覆盖的新皮层。记录同时从这三个结构中获得的MAM暴露的大鼠和完整的动物的切片制剂。采用浸浴或全身注射荷包牡丹碱诱导癫痫样活动。在离体脑片上，癫痫样放电一般起始于海马。在某些情况下，独立的PNH放电发生，但PNH从来没有“领导”在海马或新皮层放电。来自PNH神经元的细胞内记录证实，这些细胞从海马和新皮质接收突触驱动，并将轴突投射发送到这些结构-与生物胞素注射的PNH细胞的解剖学观察一致。在完整的动物制剂中，荷包牡丹碱注射在所有实验中导致癫痫样放电，通常在药物注射后2-3分钟内开始发作样电图活动。在几乎所有的动物中，发作被视为同步跨PNH，海马，和新皮层电极;在少数情况下，PNH电极（组织学证实）没有参与，但在任何情况下，在PNH电极的活动启动。发作间期放电也在所有三个电极上同步;同样，PNH从不“引导”其他两个电极，并且通常跟随（在海马/新皮层放电开始后几毫秒开始）。这些结果不支持PNH病变是原发性癫痫发生部位的假设，因为它不会引发或导致随后传播到其他脑区的癫痫样活动。
Periventricular nodular heterotopia (PNH) are, in humans, often associated with difficult-to-control epilepsy. However, there is considerable controversy about the role of the PNH in seizure generation and spread. To study this issue, we have used a rat model in which injection of methylazoxymethanol (MAM) into pregnant rat dams produces offspring with nodular heterotopia-like brain abnormalities. Electrophysiological methods were used to examine the activity of the MAM-induced PNH relative to activity in the neighboring hippocampus and overlying neocortex. Recordings were obtained simultaneously from these three structures in slice preparations from MAM-exposed rats and in intact animals. Bath application or systemic injection of bicuculline was used to induce epileptiform activity. In the in vitro slice, epileptiform discharge was generally initiated in hippocampus. In some cases, independent PNH discharge occurred, but the PNH never “led” discharges in hippocampus or neocortex. Intracellular recordings from PNH neurons confirmed that these cells received synaptic drive from both hippocampus and neocortex, and sent axonal projections to these structures – consistent with anatomical observations on biocytin-injected PNH cells. In intact animal preparations, bicuculline injection resulted in epileptiform discharge in all experiments, with a period of ictal-like electrographic activity typically initiated within 2-3 minutes after drug injection. In almost all animals, the onset of ictus was seen synchronously across PNH, hippocampal, and neocortical electrodes; in a few cases, the PNH electrode (histologically confirmed) did not participate, but in no case was activity initiated in the PNH electrode. Interictal discharge was also synchronized across all three electrodes; again, the PNH never “led” the other two electrodes, and typically followed (onset several milliseconds after hippocampal/neocortical discharge onset). These results do not support the hypothesis that the PNH lesion is the primary epileptogenic site since it does not initiate or lead epileptiform activity that subsequently propagates to other brain regions.
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