Neuroprotection in a model of chronic ocular hypertension

当血液供应减少时，视网膜和大脑等神经组织可能会受到损害。这可能发生在眼睛疾病，青光眼，其中眼睛内的压力升高。这种严重的情况往往导致失明。许多神经元损伤被认为是由于过量谷氨酸的释放。谷氨酸是一种化学物质（神经递质），神经用来相互交流，但它在高浓度时对神经有毒。该项目将利用一种新的青光眼模型来研究调节视网膜中谷氨酸浓度的机制。如果这些机制能够更有效地发挥作用，它们可能会阻止谷氨酸的积累，从而防止对神经细胞的损害。了解这些机制将有助于开发一种有效的治疗方法，以防止15万澳大利亚青光眼患者的视力丧失。

Damage can occur to nervous tissues like the retina and brain when there is a reduction in the blood supply. This can occur in the eye disease, glaucoma, in which the pressure inside the eye is elevated. This serious condition often results in blindness. Much of the neuronal damage is thought to be due to the release of an excess of glutamate. Glutamate is a chemical (neurotransmitter) that nerves use to communicate with each other, but it is toxic to nerves when present at high concentrations. This project will utilise a new model of glaucoma to investigate the mechanisms that regulate the concentration of glutamate in the retina. If these mechanisms could be made to work more efficiently, they may prevent the build-up of the glutamate and therefore prevent damage to the nerve cells. Understanding these mechanisms will aid in the development of an effective treatment to prevent visual loss in the 150,000 Australians who suffer from glaucoma.