Neuroprotection in a model of chronic ocular hypertension

慢性高眼压模型的神经保护作用

• 批准号: nhmrc : 401529
• 负责人: A/Pr Nigel Barnett
• 金额: $ 17.62万
• 依托单位: The University of Queensland
• 依托单位国家: 澳大利亚
• 项目类别: NHMRC Project Grants
• 财政年份: 2006
• 资助国家: 澳大利亚
• 起止时间: 2006-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://researchdata.edu.au/neuroprotection-model-chronic-ocular-hypertension/94344
• 关键词: Neuroprotection; model; chronic; ocular; hypertension

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.

当血液供应减少时，视网膜和大脑等神经组织会受到损害。这可能发生在眼病，青光眼，其中眼内压力升高。这种严重的情况通常会导致失明。大部分神经元损伤被认为是由于过量释放谷氨酸所致。谷氨酸是一种化学物质（神经递质），神经用它来相互交流，但当谷氨酸浓度很高时，它对神经是有毒的。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有效的治疗方法，以防止澳大利亚15万名青光眼患者的视力丧失。