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

我们研究了TrkB受体在正常大鼠和缺氧/缺血损伤幼鼠大脑皮层中的表达。TrkB表达细胞在出生时存在于梨状皮质中，并且数量增加，出现在整个大脑皮质中。P30时TrkB细胞密度达到成体水平。形态学上分为锥体神经元和中间神经元。缺氧/缺血损伤诱导TrkB全长受体的试探性上调。在梗死周围区观察到TrkB表达细胞的新形态和细胞体和树突上的免疫染色增强，在动脉结扎的对侧皮质中检测到表达TrkB的神经元数量增加。缺氧48小时后，这种上调不再明显。GFA、OX-42或carbinine - d28抗血清的双重免疫染色显示TrkB受体与这些分子没有共定位。损伤反应水平的改变表明TrkB可能通过配体BDNF在缺氧/缺血性损伤神经元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.