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脑回小多畸形中抑制性中间神经元分布的改变。

Altered distribution of inhibitory interneurons in polymicrogyria.

机构信息

Department of Pediatrics, Shiga University of Medical Science, Seta-Tsukinowa, Otsu 520-2192, Japan.

出版信息

Epilepsy Res. 2012 Nov;102(1-2):113-6. doi: 10.1016/j.eplepsyres.2012.05.001. Epub 2012 May 28.

DOI:10.1016/j.eplepsyres.2012.05.001
PMID:22647842
Abstract

There is a high incidence of epilepsy in patients with polymicrogyria; however, the epileptogenic mechanisms are largely unknown. The density of parvalbumin-immunoreactive interneurons was evaluated in an experimental model of polymicrogyria, in order to assess the potential changes in the development of one population of inhibitory interneurons. Newborn hamsters received an intracerebral injection of ibotenate, and all injected animals showed abnormal cortical layers characterized by one or two microgyrus in the fronto-parietal cortex. A quantitative analysis revealed that the ratios of parvalbumin-immunoreactive neurons in total neurons were significantly reduced in the medial paramicrogyral area, and in the medial and central parts of microgyrus in comparison to that in the lateral part of microgyrus (P<0.01). The lateral paramicrogyral area had the greatest number of parvalbumin-immunoreactive neurons, which was increased significantly in comparison to that in the control cortex (P<0.01). We suggest that the callosal, thalamic and intracortical afferents to the microgyrus and paramicrogyral area may induce a remarkable imbalance between the excitatory and inhibitory activities of the cortical structures, associated with the epileptogenic mechanism in polymicrogyria.

摘要

多微小脑回畸形患者癫痫发病率较高,但致痫机制尚不清楚。本研究通过建立多微小脑回畸形动物模型,评估抑制性中间神经元发育的潜在变化,观察颗粒蛋白免疫反应阳性中间神经元的密度变化。新生仓鼠接受海人酸脑内注射,所有注射动物均在前顶叶皮质出现一个或两个微脑回的异常皮质层。定量分析显示,与微脑回外侧部相比,内侧旁微脑回区和微脑回的内侧及中央部颗粒蛋白免疫反应阳性神经元与总神经元的比例显著降低(P<0.01)。旁微脑回区颗粒蛋白免疫反应阳性神经元数量最多,与对照组皮质相比显著增加(P<0.01)。我们推测,微脑回和旁微脑回区的放射冠、丘脑和皮质内传入纤维可能导致皮质结构的兴奋性和抑制性活动之间出现显著失衡,这与多微小脑回畸形的致痫机制有关。

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引用本文的文献

1
Pathophysiology of epileptic encephalopathies.癫痫性脑病的病理生理学。
Epilepsia. 2013 Nov;54 Suppl 8(0 8):6-13. doi: 10.1111/epi.12417.