Changes in Calcium-Binding Protein Expression in Human Cortical Contusion Tissue
Changes in Calcium-Binding Protein Expression in Human Cortical Contusion Tissue
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DOI：
10.1089/neu.2009.0894
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发表时间：
2009-12-01
影响因子：
4.2
通讯作者：
Pimienta, Heman J.
中科院分区：
文献类型：
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作者：
Buritica, Efrain;Villamil, Liliana;Pimienta, Heman J.
创伤性脑损伤 (TBI) 会产生多种细胞变化，例如神经胶质增生、轴突和树突可塑性、抑制-兴奋不平衡以及细胞死亡，这些变化可能引发癫痫发生。研究表明，实验模型中大脑皮质损伤后抑制成分的功能障碍可能导致癫痫持续状态；我们建议分析人类 TBI 后皮质中间神经元和星形胶质细胞的反应。对 12 个挫伤样本进行了评估，确定了胶质原纤维酸性蛋白 (GFAP) 和钙结合蛋白 (CaBP) 的表达。该研究是在保留和不保留细胞结构的区域中进行的，并使用 NeuN 免疫反应性 (IR) 进行评估。在 NeuN-IR 完全丧失的区域中，结果显示神经纤维和体细胞中 CaBP-IR 均显着丧失。在具有保守细胞结构的区域中，检测到 CaBP-IR 的剧烈变化较小。这些变化包括第二层小清蛋白 (PV-IR) 神经元数量减少、第三层和第五层钙结合蛋白 (CB-IR) 神经元数量增加以及第二层钙结合蛋白 (CR-IR) 神经元数量增加。我们还在白质、灰白质转变以及 NeuN-IR 完全丧失的区域周围观察到了胶质纤维酸性蛋白免疫反应性 (GFAP-IR)。这些发现可能反映了病变导致的动态活动，该病变与邻近过度活跃的谷氨酸能神经元的兴奋回路的变化有关，可能是由于主要影响或缺氧缺血等次要事件。这些变化的时间演变可能是将严重皮质挫伤与在一些患者中观察到的致癫痫活动联系起来的基础。
Traumatic brain injury (TBI) produces several cellular changes, such as gliosis, axonal and dendritic plasticity, and inhibition-excitation imbalance, as well as cell death, which can initiate epileptogenesis. It has been demonstrated that dysfunction of the inhibitory components of the cerebral cortex after injury may cause status epilepticus in experimental models; we proposed to analyze the response of cortical interneurons and astrocytes after TBI in humans. Twelve contusion samples were evaluated, identifying the expression of glial fibrillary acidic protein (GFAP) and calcium-binding proteins (CaBPs). The study was made in sectors with and without preserved cytoarchitecture evaluated with NeuN immunoreactivity (IR). In sectors with total loss of NeuN-IR the results showed a remarkable loss of CaBP-IR both in neuropil and somata. In sectors with conserved cytoarchitecture less drastic changes in CaBP-IR were detected. These changes include a decrease in the amount of parvalbumin (PV-IR) neurons in layer II, an increase of calbindin (CB-IR) neurons in layers III and V, and an increase in calretinin (CR-IR) neurons in layer II. We also observed glial fibrillary acidic protein immunoreactivity (GFAP-IR) in the white matter, in the gray-white matter transition, and around the sectors with NeuN-IR total loss. These findings may reflect dynamic activity as a consequence of the lesion that is associated with changes in the excitatory circuits of neighboring hyperactivated glutamatergic neurons, possibly due to the primary impact, or secondary events such as hypoxia-ischemia. Temporal evolution of these changes may be the substrate linking severe cortical contusion and the resulting epileptogenic activity observed in some patients.