Nodule excitability in an animal model of periventricular nodular heterotopia: c-fos activation in organotypic hippocampal slices.
Nodule excitability in an animal model of periventricular nodular heterotopia: c-fos activation in organotypic hippocampal slices.
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DOI：
10.1111/epi.12945
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发表时间：
2015-04
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：
Doisy ET;Wenzel HJ;Mu Y;Nguyen DV;Schwartzkroin PA
大脑发育异常可能导致结构发育不良，例如脑室周围结节。虽然这些异常的神经元集合通常与难以控制的癫痫活动有关，但对于结节本身的致癫痫性却几乎没有达成共识。由于一种常见的治疗选择是手术切除可疑的癫痫结节，因此确定这些结构是否确实引起或基本上导致癫痫活动非常重要。为了研究异常结节的兴奋性，我们检查了器官型海马切片培养物中 c-fos 的激活情况，该培养物是通过用甲基偶氮甲醇处理怀孕大鼠而创建的脑室周围结节异位动物模型产生的。使用这种制剂，我们还尝试评估通过手术从培养物中取出结节时的组织兴奋性。然后，我们将这种体外制剂中的 c-fos 激活与用红藻氨酸处理的完整大鼠中产生的 c-fos 激活进行了比较。与新皮质或 CA1 海马相比，c-fos 激活的定量分析未能显示结节兴奋性增强。然而，当我们比较有结节和没有结节的培养物时，结节的存在确实影响 CA1 和皮质的兴奋性，至少如 c-fos 标记所反映的那样。手术切除结节并没有导致 c-fos 生物标志物所反映的兴奋性持续下降。我们的器官型培养结果总体上与我们对完整大鼠兴奋性的观察结果一致——不仅在 c-fos 中如此，而且在之前的电生理学研究中也如此。至少在这个模型中，结节似乎并不导致兴奋性增强（或者可能导致癫痫发作）。含有结节的组织的兴奋性是不同的，这表明网络功能发生了改变，可能反映了产生结节的异常发育模式。
Aberrations in brain development may lead to dysplasic structures such as periventricular nodules. While these abnormal collections of neurons are often associated with difficult-to-control seizure activity, there is little consensus regarding the epileptogenicity of the nodules themselves. Since one common treatment option is surgical resection of suspected epileptic nodules, it is important to determine whether these structures in fact give rise, or essentially contribute, to epileptic activities. To study the excitability of aberrant nodules, we have examined c-fos activation in organotypic hippocampal slice cultures generated from an animal model of periventricular nodular heterotopia created by treating pregnant rats with methylazoxymethanol. Using this preparation, we have also attempted to assess tissue excitability when the nodule is surgically removed from the culture. We then compared c-fos activation in this in vitro preparation to c-fos activation generated in an intact rat treated with kainic acid. Quantitative analysis of c-fos activation failed to show enhanced nodule excitability compared to neocortex or CA1 hippocampus. However, when we compared cultures with and without a nodule, presence of a nodule did affect the excitability of CA1 and cortex, at least as reflected in c-fos labeling. Surgical removal of the nodule did not result in a consistent decrease in excitability as reflected in the c-fos biomarker. Our results from the organotypic culture were generally consistent with our observations on excitability in the intact rat – as seen not only with c-fos but also in previous electrophysiological studies. At least in this model, the nodule does not appear to be responsible for enhanced excitability (or, presumably, seizure initiation). Excitability is different in tissue that contains a nodule, suggesting altered network function, perhaps reflecting the abnormal developmental pattern that gave rise to the nodule.
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影响因子：
5.6
作者：
Battaglia, G;Granata, T;Avanzini, G
通讯作者：
Avanzini, G
DOI：
10.1016/j.yebeh.2013.08.028
发表时间：
2013-11
期刊：
Epilepsy & behavior : E&B
影响因子：
--
作者：
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影响因子：
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作者：
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作者：
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影响因子：
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作者：
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