Loss of hilar mossy cells in Ammon's horn sclerosis
Loss of hilar mossy cells in Ammon's horn sclerosis
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DOI：
10.1111/j.1528-1157.2000.tb01577.x
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发表时间：
2000-01-01
期刊：
影响因子：
5.6
通讯作者：
Wiestler, OD
中科院分区：
文献类型：
--
作者：
Blümcke, I;Suter, B;Wiestler, OD
目的：门苔藓细胞是海马结构重要的兴奋性细胞亚群。几项研究已经确定这种细胞类型特别容易在边缘癫痫大鼠模型的癫痫发作活动。方法：对30例慢性颞叶癫痫（TLE）患者的海马标本进行形态学和免疫组化分析，其中21例表现为节段性神经元细胞丢失[阿蒙角硬化（AHS）]，8例表现为不累及海马的局灶性病变（肿瘤、瘢痕、畸形）。在另外一名TLE患者中，未观察到组织病理学改变。无癫痫的肿瘤患者（n = 2）和非癫痫尸检脑（n = 8）的手术标本作为对照。使用针对代谢型谷氨酸受体亚型mGluR7b的新型多克隆抗血清或通过细胞内荧光黄注射来可视化人海马中的门苔藓细胞。结果：与对照组相比，AHS患者mGluR7免疫反应阳性苔藓细胞明显减少（p < 0.05）。相反，有局灶性病变但海马结构完整的TLE患者仅表现出这种神经元亚群的离散的、非显著的减少。这一观察结果通过分析来自AHS患者的62个随机注射的肺门神经元得到证实，其中我们无法检测到具有类似于肺门苔藓细胞的形态的神经元。我们目前的数据表明，在伴有AHS的TLE患者中，肺门苔藓细胞明显丢失。相比之下，肺门苔藓细胞似乎是不太脆弱的病变相关的TLE患者。虽然mGluR7在苔藓细胞中的免疫反应性的意义仍有待研究，但该细胞群的丧失与海马网络的改变和区域性过度兴奋作为AHS和TLE的致病机制是相容的。
Purpose: Hilar mossy cells represent an important excitatory subpopulation of the hippocampal formation. Several studies have identified this cell type as particularly vulnerable to seizure activity in rat models of limbic epilepsy. Hen we have subjected hilar mossy cell loss in the hippocampus of patients with chronic temporal lobe epilepsy (TLE) to a systematic morphological and immunohistochemical analysis.Methods: Hippocampal specimens from 30 TLE patients were included; 21 patients presented with segmental neuronal cell loss [Ammon's horns clerosis (AHS)] and 8 with focal Lesions (tumors, scars, malformations) not involving the hippocampus proper. In one additional TLE patient, no histopathological alteration could be observed. Surgical specimens from tumor patients without epilepsy (n = 2) and nonepileptic autopsy brains(n = 8) were used as controls. Hilar mossy cells in the human hippocampus were visualized using a novel poly cloncal antiserum directed against the metabotropic glutamate receptor subtype mGluR7b or by intracellular Lucifer Yellow injection. confocal laser scanning microscopy, and three-dimensional morphological reconstruction.Results: Compared with controls, a significant loss of mGluR7 immunoreactive mossy cells was observed in patients with AHS (p < 0.05). In contrast, TLE patients with focal lesions but structurally intact hippocampus demonstrated only a discrete, nonsignificant reduction of this neuronal subpopulation, This observation was confirmed by analysis of 62 randomly injected hilar neurons from AHS patients, in which we were unable to detect neurons with a morphology like that of hilar mossy cells.Conclusion: Our present data indicate significant hilar mossy cell loss in TLE patients with AHS. In contrast, hilar mossy cells appear to be less vulnerable in patients with lesion-associated TLE. Although the significance of mGluR7 immunoreactivity in mossy cells remains to be studied, loss of this cell population is compatible with alterations in hippocampal networks and regional hyperexcitability as pathogenic mechanism of AHS and TLE.