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

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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.