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This dissertation, Differential Expression of P75 Low Affinity Neurotrophin Receptor in Hypoxic-ischemic Neonatal Mouse Brain by 林國泰, Kwok-tai, Lam, was obtained from The University of Hong Kong (Pokfulam, Hong Kong) and is being sold pursuant to Creative Commons: Attribution 3.0 Hong Kong License. The content of this dissertation has not been altered in any way. We have altered the formatting in order to facilitate the ease of printing and reading of the dissertation. All rights not granted by the above license are retained by the author. Abstract: Abstract of thesis entitled Differential Expression of p75 Low Affinity Neurotrophin Receptor in Hypoxic-Ischemic Neonatal Mouse Brain Submitted by Lam Kwok Tai For the degree of Master of Philosophy At the University of Hong Kong In December 1998 We had adopted the unilateral common carotid artery ligation followed by hypoxia model to study hypoxic-ischemic (HI) encephalopathy in 7 days old mice. The damage to the HI brains was characterized by 2,3,5-tri-phenyltetrazoliurn chloride (TTC), haematoxylin and eosin (H&E) stain, and TUNEL assay. We also investigated the possible alteration of p75 low affinity nerve growth factor receptor (p75NGFR) in the neonatal mice brains after HI insults. To further explore the role of p75NGFR in neonatal HI encephalopathy, we subjected p75NGFR targeted mutated mice to the same HI treatment and examination procedures. TTC staining of brains at 1 day after HI showed that the damage was grossly limited to the side ipsilateral to ligation. The sensitivities of different brain regions to HI damage were in the following decreasing order: posterior cortex, hippocampus, anterior cortex, striatum and thalamus. Histomorphological analysis of H&E stained brain sections from 1 hr, 3 hr, and 1,2, 3 and 4 days post-HI revealed that the damage areas peaked early at 3 hr. The damage subsided rapidly by day 2 and further diminished by day 4. On the other hand, TUNEL assay of the anterior hippocampal brain sections from these same H&E stained brains revealed that apoptotic cells were substantially increased on the ipsilateral side by 1 and 2 day post-HI. By day 3 and 4 post-HI, the apoptotic cells decreased drastically but maintaining the difference between the contralateral and ipsilateral sides. There were no difference between the two sides of the HI brains at 3 hr after HI, suggesting a delayed phase of neuronal cell death had occurred beyond this time point. The expression of p75NGFR, studied by immunohistochemistry, was decreased in the core-damaged area of the cortex and hippocampus by 1 hr and remained low at 3, 6 hr and 1, 3 days post HI insult. The perifocal areas maintained a normal expression of p75NGFR comparable to the contralateral side at 1, 3 and 6 hours but was increased at 3 and 4 days post HI. Additionally, the corresponding cortical subplate showed cells with intensified p75NGFR expression while the p75NGFR positive axonal tracks running radially through the cortex were suppressed. By 7 days after HI, p75NGFR expressions, which decreased with advancing age in early postnatal development, were equalized in both the ipsilateral and contralateral sides. Such differential temporal and spatial p75NGFR expression after HI insult may reflect its active role inneonatal hypoxic-ischemic encephalopathy (HIE) in mice. The p75NGFR null mutated mice showed no observable damage by TTC at 1 day after HI. The H&E stain and TUNEL assay revealed that these mice had substantially less affected cells than the wild type mice. Interestingly, contrast to the wild type mice HI vulnerable brain regions such as hippocampus and the cortex were spared while other areas like the lateral geniculate body and thalamus revealed higher densities of damaged cells. Thus the lack of functional p75NGFR might reduce the susceptibility of brain cells to HI damage, further suggesting that p75NGFR is involved in neonatal HIE. It is reasonable to speculate that det

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