Expression of TrkB and BDNF in human cochlea-an immunohistochemical study
Expression of TrkB and BDNF in human cochlea-an immunohistochemical study
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DOI：
10.1007/s00441-011-1209-3
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发表时间：
2011-08-01
影响因子：
3.6
通讯作者：
Rask-Andersen, Helge
中科院分区：
文献类型：
--
作者：
Liu, Wei;Kinnefors, Anders;Rask-Andersen, Helge
手术的人耳蜗标本，获得在通过经耳蜗的方法，其中耳蜗被删除的最大限度地暴露的肿瘤和保护的重要结构，如脑干，颅神经，和中枢血管的大型后颅窝脑膜瘤切除。耳蜗组织固定后冰冻切片，进行酪氨酸激酶受体B（Trk B）和脑源性神经营养因子（BDNF）免疫组织化学染色。TrkB受体蛋白在人螺旋神经节神经元胞体和突起中均有表达。在人体Corti器官中，TrkB免疫反应性主要存在于外毛细胞下面的神经纤维中。BDNF在Corti器和耳蜗螺旋神经节中均无表达。为了抗体特异性以及为了对照和比较的目的，在来自成年豚鼠的耳蜗神经元/神经胶质的原代培养物中进行TrkB免疫细胞化学。共聚焦激光扫描显微镜显示TrkB均匀分布于神经元胞体和轴突的胞浆中。了解TrkB受体在人耳蜗中的表达有助于确定听力受损患者神经元保护的靶结构。我们的研究结果表明，在病理条件下SGNs的再生可以增强BDNF/TrkB为基础的药物或遗传策略。
Surgical human cochlear specimens were obtained during the removal of large posterior cranial fossa meningioma by a transcochlear approach in which the cochlea was removed for maximal exposure of the tumor and protection of important structures, such as the brainstem, cranial nerves, and pivotal blood vessels. The cochlear tissue was fixed and cryo-sectioned for tyrosine kinase receptor B (TrkB) and brain-derived neurotrophic factor (BDNF) immunohistochemistry. TrkB receptor protein was expressed in both neuronal somata and the processes of human spiral ganglion neurons (SGNs). In the human organ of Corti, TrkB immunoreactivity was mainly present in nerve fibers underneath outer hair cells. BDNF expression was found neither in the organ of Corti nor in the spiral ganglion of human cochlea. For antibody specificity and for control and comparative purposes, TrkB immunocytochemistry was performed in primary cultures of cochlear neuron/glia from adult guinea pig. Confocal laser scanning microscopy showed that TrkB was homogeneously distributed in the cytoplasm of both neuronal somata and axons. Knowledge of the expression of TrkB receptor in human cochlea should help to determine the target structures for neuron preservation in hearing-impaired patients. Our results indicate that the regeneration of SGNs under pathological conditions can be enhanced with BDNF/TrkB-based pharmaceutical or genetic strategies.