Hippocampus/amygdala alterations, loss of heparan sulfates, fractones and ventricle wall reduction in adult BTBR T+ tf/J mice, animal model for autism.
Hippocampus/amygdala alterations, loss of heparan sulfates, fractones and ventricle wall reduction in adult BTBR T+ tf/J mice, animal model for autism.
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成年 BTBR T tf/J 小鼠海马/杏仁核的改变、硫酸乙酰肝素的损失、分形蛋白和心室壁的减少，自闭症动物模型。
DOI：
10.1016/j.neulet.2011.11.007
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发表时间：
2012
影响因子：
2.5
通讯作者：
Douet,Vanessa
中科院分区：
文献类型：
--
作者：
Mercier,Frederic;Kwon,YoungsuCho;Douet,Vanessa
多项研究表明，海马体和杏仁核的改变与自闭症的病理学有关。我们以前曾报道解剖学改变脑膜，血管和fractones，专门的细胞外基质（ECM）的室下区，在成年BTBR T+ tf/J小鼠，自闭症的动物模型的前脑。在这里，我们使用bisbenzidine细胞核染色和双重免疫荧光组织化学层粘连蛋白和N-硫酸乙酰肝素硫酸蛋白多糖（NS-HSPG）检查一系列的大脑切片，包含杏仁核和海马在成年BTBR T+ tf/j小鼠。我们观察到两个脑脊膜过度分离，脑膜的轨迹改变导致侧脑室脉络丛萎缩，齿状回颗粒层变短，杏仁核尺寸减小。杏仁核侧脑室、第三脑室萎缩。在整个第三脑室和侧脑室壁，碎片的数量和大小，以及它们对NS-HSPG的免疫反应性降低。在虹膜状皮质/杏仁核界面处发现血管扩张。这些结果显示了海马/杏仁核的解剖学改变，其与BTBR T+ TF/J小鼠中脉络丛/心室系统和ECM的缺陷相关。在患有自闭症的人类中海马/杏仁核轴的类似改变与在BTBR T+ tf/J小鼠中观察到的类似改变使得该动物模型对于自闭症的研究非常有价值。此外，BTBR T+ Tf/J小鼠的脑膜/血管和ECM的改变表明自闭症中脑结缔组织的可能作用。
Multiple studies converge to implicate alterations of the hippocampus and amygdala in the pathology of autism. We have previously reported anatomical alterations of the meninges, vasculature and fractones, the specialized extracellular matrix (ECM) of the subventricular zone, in the forebrain of adult BTBR T+ tf/J mice, animal model for autism. Here, we used bisbenzidine cell nucleus staining and dual immunofluorescence histochemistry for laminin and N-sulfated heparan sulfate proteoglycans (NS-HSPG) to examine a series of brain sections containing the amygdala and hippocampus in the adult BTBR T+ tf/j mouse. We observed an excessive separation of the two hippocampi, a modified trajectory of the meninges leading to a shrunken choroid plexus in the lateral ventricle, a shorter granular layer of the dentate gyrus, and a reduced size of the amygdala nuclei. The lateral ventricle near the amygdala, and the third ventricle were shrunken. The number and size of fractones, and their immunoreactivity for NS-HSPG, were reduced throughout the third and lateral ventricles walls. Enlarged blood vessels were found at the endopiriform cortex/amygdala interface. These results show anatomical alterations of the hippocampal/amygdala that are associated with defects of the choroid plexus/ventricular system and the ECM in the BTBR T+ TF/J mouse. Similar alterations of the hippocampus/amygdala axis in humans with autism to these observed in BTBR T+ tf/J mice make this animal model highly valuable for the study of autism. Moreover, the meningo/vascular and ECM alterations in BTBR T+ Tf/J mice suggest a possible role of the brain connective tissue in autism.