Quantitative analysis of parvalbumin-immunoreactive cells in the human epileptic hippocampus
Quantitative analysis of parvalbumin-immunoreactive cells in the human epileptic hippocampus
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DOI：
10.1016/j.neuroscience.2007.07.029
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发表时间：
2007-10-12
期刊：
影响因子：
3.3
通讯作者：
Defelipe, J.
中科院分区：
文献类型：
--
作者：
Andrioli, A.;Alonso-Nanclares, L.;Defelipe, J.
海马硬化是顽固性颞叶癫痫患者中最常见的病理，主要涉及海马神经元丢失和神经胶质瘤。这些变化伴随着存活神经元中各种分子表达的变化，以及兴奋和抑制回路中的轴突重组。表达钙结合蛋白小白蛋白（PV）的gaba能中间神经元亚群的改变被认为是癫痫发生过程中的关键因素。我们研究了伴有和不伴有硬化症的癫痫患者手术切除的海马组织中细小蛋白免疫反应（PV-ir）神经元的分布和密度。利用定量体视学方法，我们首次发现在任何海马区，神经元总损失与PV-ir神经元损失之间没有相关性。我们还观察到，与非硬化性癫痫和尸检海马相比，硬化性枕下的总神经元密度较高，同时PV-ir密度较低。这些结果表明，硬化患者表面正常的枕骨下，PV-ir神经元的密度和比例也发生了意想不到的变化。(c) 2007年Elsevier Ltd代表IBRO出版。
Hippocampal sclerosis is the most frequent pathology encountered in mesial temporal structures resected from patients with intractable temporal lobe epilepsy and it mainly involves hippocampal neuronal loss and gliosis. These alterations are accompanied by changes in the expression of a variety of molecules in the surviving neurons, as well as axonal reorganization in both excitatory and inhibitory circuits. The alteration of a subpopulation of GABAergic interneurons that expresses the calcium binding protein parvalbumin (PV) is thought to be a key factor in the epileptogenic process. We investigated the distribution and density of parvalbumin-immunoreactive (PV-ir) neurons in surgically resected hippocampal tissue from epileptic patients with and without sclerosis. Using quantitative stereological methods, we show for the first time that there is no correlation between total neuronal loss and PV-ir neuronal loss in any of the hippocampal fields. We also observed higher values of the total neuronal density in the sclerotic subiculum, which is accompanied by a lower density of PV-ir when compared with non-sclerotic epileptic and autopsy hippocampi. These findings suggest that, the apparently normal subiculum from sclerotic patients also shows unexpected changes in the density and proportion of PV-ir neurons. (c) 2007 Published by Elsevier Ltd on behalf of IBRO.