Regulation of synaptic inhibition by GABAA receptor trafficking under normal conditions and in neurological and neuropsy

正常条件下以及神经病学和神经病理学中 GABAA 受体运输对突触抑制的调节

• 批准号: G0802377/1
• 负责人: Josef Kittler
• 金额: $ 246.4万
• 依托单位: University College London
• 依托单位国家: 英国
• 项目类别: Fellowship
• 财政年份: 2009
• 资助国家: 英国
• 起止时间: 2009 至 无数据
• 项目状态: 已结题
• 来源: https://gtr.ukri.org/projects?ref=G0802377%2F1
• 关键词: Regulation; synaptic; inhibition; GABAA; receptor

Nerve cells send signals to each other by releasing chemicals called neurotransmitters at special sites called synapses. The neurotransmitters act on special proteins (receptors), allowing ions to cross the cell membrane, thus producing voltage changes across the membrane. My application is on two key aspects of brain function: (i) how neurons regulate the number of neurotransmitter receptor proteins present at synapses to control the size of the membrane voltage changes; and (ii) how this regulation may be altered in disease processes. Studying the molecular mechanisms that underlie these regulatory processes will allow us to understand better how the brain works under healthy conditions, and how dysregulation of these processes leads to altered electrical behaviour of nerve cells in disease. This work could lead the way to the development of new therapies in devastating diseases such as epilepsy, stroke, anxiety, Huntington‘s disease, substance abuse, depression, Parkinson‘s disease and autism.

神经细胞通过在称为突触的特殊部位释放称为神经递质的化学物质来相互发送信号。神经递质作用于特殊的蛋白质（受体），允许离子穿过细胞膜，从而产生跨膜电压变化。我的申请是关于大脑功能的两个关键方面：（i）神经元如何调节突触上存在的神经递质受体蛋白的数量，以控制膜电压变化的大小;以及（ii）这种调节如何在疾病过程中改变。研究这些调节过程的分子机制将使我们更好地了解大脑在健康条件下如何工作，以及这些过程的失调如何导致疾病中神经细胞的电行为改变。这项工作可能会导致开发新的治疗方法，用于治疗癫痫、中风、焦虑、亨廷顿病、药物滥用、抑郁症、帕金森病和自闭症等毁灭性疾病。