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This dissertation, Functional Changes and Differential Cell Death of Retinal Ganglion Cells After Injury by Suk-yee, Li, 李淑儀, 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 Functional Changes and Differential Cell Death of Retinal Ganglion Cells after Injury Submitted by Suk-Yee LI for the degree of Doctor of Philosophy at the University of Hong Kong in April 2007 Retinal ganglion cells (RGCs) and optic nerves are parts of the central nervous system (CNS) that are engaged in the visual function. The regeneration ability of CNS neurons is restricted by several intrinsic and extrinsic factors. Therefore, the investigation on protecting the RGCs and the optic nerves following injury is crucial to prevent visual impairments. Experimental ocular hypertension (OH) and optic nerve transection (ONT) models are two approaches commonly used to mimic the degeneration of RGCs and optic nerves. In the first part of the study, OH was induced using laser photocoagulation on the episcleral veins and limbal veins of rats to monitor the functional changes of retina using electroretinography (ERG) as the tool. The attenuation of the components in the ERG gives the fundamental information on the decrease of RGC activities in this particular model. Progressive deterioration of retinal function and RGC degeneration are noticed following the injury of RGCs and optic nerves, implying that some of the RGCs lose function and died before the others. However, the factors that attribute to the delayed cell death of RGCs are still under investigation. Recently, a novel photopigment, melanopsin, is found to express exclusively in a sub-population of RGCs that project their axons to the suprachiasmatic nucleus and modulates the photoentrainment. The most striking result from the present study is that these melanopsin-expressing RGCs (mRGCs) are found to be less susceptible to both OH and ONT insults compared to those do not express melanopsin. This observation provides a model for exploring the factors that protect the mRGCs from damage. The phosphoinositide 3-kinase (PI3K) signalling pathway is one of the survival mechanisms and plays an important role in protecting RGCs from the apoptotic cell death. Activation of Protein Kinase B (PKB or Akt), the downstream effector of PI3K, is found to be expressed in the surviving cells following the RGC injury suggesting that the delayed cell death of mRGCs may be due to the involvement of the PI3K/Akt survival pathway. Surprisingly, a group of the surviving mRGCs after ONT also expressed pAkt. To further verify this fact, application of the specific PI3K inhibitors is performed to inhibit this survival mechanism. Application of the PI3K inhibitors, LY294002 and Wortmannin, significantly decreased the survival of mRGCs following both types of injuries. The data herein imply that the survival of mRGCs probably goes through the PI3K/Akt signalling pathway. The present study provides more insights on the death profile of mRGCs under both chronic and acute insults. Also, the underlying factors attributing to the intrinsic delayed cell death of mRGCs not only give hints on using the mRGCs as a tool to study the differential cell injury of RGCs, but also open a new area for future study to understand more on the mRGCs. (458 words) DOI: 10.5353/th_b3859773 Subjects: ApoptosisRetinal ganglion cellsOptic nerve - Wounds and injuriesRetinal degeneration

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