EXPERIMENTAL STUDY ON ROLES OF NEUROTROPHIC FACTOR IN NEONATAL HYPOXIC/ISCHEMIC ENCEPHALOPATYH

本实验研究了TrkB受体在正常大鼠和缺氧缺血性损伤幼鼠大脑皮质中的表达。TrkB表达细胞在出生时存在于梨状皮质中，并且数量增加并出现在整个大脑皮质中。TrkB细胞密度在P30时达到成体水平。它们在形态学上被认为是锥体神经元和中间神经元。缺氧/缺血性损伤诱导全长TrkB受体的初步上调。在梗塞周围区域中观察到TrkB表达细胞的新外观和细胞体和树突上增强的免疫染色，并且在动脉结扎的对侧皮质中检测到TrkB表达神经元的数量增加。这种上调在缺氧48小时后不再明显。使用抗GFA、OX-42或卡宾胺-D28的抗血清的双重免疫染色显示TrkB受体和这些分子没有共定位。TrkB在神经元缺氧缺血性损伤中的表达变化提示TrkB可能通过配体BDNF在神经元缺氧缺血性损伤的早期保护机制中发挥重要作用。

We studied the expression of TrkB receptor in the cerebral cortex of normal rats and of the young rats with hypoxic/ischemic injury. TrkB expressing cells existed in the piriform cortex at birth and increased in number and emerged in the entire cerebral cortex. Density of TrkB cells reached to adult level at P30. They were morphologically regarded as pyramidal neurons and interneurons. Hypoxic/ischemic injury induced tentative upregulation of full-length TrkB receptor. Novel appearance of TrkB expressing cells and enhanced immunostain on both cell bodies and dendrites were observed in the peri-infarct areas and increased number of TrkB expressing neurons was detected in the contralateral cortex to artery ligation. This upregulation was no more evident after 48 hr of hypoxia. The double immunostaining using antiserum against GFA,OX-42 or carbindine-D28 revealed no co-localization of TrkB receptor and these molecules. The altered levels in responses to injury indicate that TrkB may crucial roles in early protective mechanism of the neurons with hypoxic/ischemic injury through ligands BDNF.