A Novel Mechanism of Calcium Efflux and Signal Decay in Adrenal Chromaffin Cells

肾上腺嗜铬细胞钙流出和信号衰减的新机制

• 批准号: 9723676
• 负责人: Allan Schneider
• 金额: $ 25.07万
• 依托单位: Albany Medical College of Union University
• 依托单位国家: 美国
• 项目类别: Standard Grant
• 财政年份: 1997
• 资助国家: 美国
• 起止时间: 1997-09-01 至 2002-08-31
• 项目状态: 已结题
• 来源: https://www.nsf.gov/awardsearch/showAward?AWD_ID=9723676&HistoricalAwards=false
• 关键词: Novel; Mechanism; Calcium; Efflux; Signal

9723676 Schneider Nerve cells communicate with each other by the release of chemical messengers or neurotransmitters, which then act on neighboring cells to complete transmission of the message. The release of the chemical neuro- transmitter is regulated by a brief rise and decay in cell calcium in the nerve endings or terminals. Whatever regulates the calcium levels in the nerve terminals will in turn regulate the rate, amount and duration of release of the chemical neurotransmitter. The objective of the present project is to clarify the mechanisms regulating the calcium signals for neurotransmitter release using a model nerve cell system known as adrenal chromaffin cells. Chromaffin cells derive from the interior of the adrenal gland and like nerves, secrete their neurohormones, adrenaline and noradrenaline, in response to a rise in cell calcium. While the cellular mechanisms regulating the rise in cell calcium are well understood, those regulating the buffering and decay of the calcium signal for secretion are not well defined. Such mechanisms are important since they in turn will regulate the strength and duration of communication between nerve cells. The present project will test a novel mechanism for regulating calcium signal decay which uses a sodium- dependent calcium transport protein to remove calcium from the cell. Such transport proteins are known as sodium- calcium exchangers and may exist in several different forms in different cellular compartments. The role and nature of the sodium-calcium exchange proteins in calcium signal decay will be determined. The project should result in an improved understanding of the cellular mechanisms regulating the calcium signal for neurotransmitter release and the identitiy of the calcium transport proteins involved in cellular calcium clearance and signal decay.

小行星9723676 神经细胞通过释放化学信使或神经递质相互交流，然后作用于相邻细胞以完成信息的传递。 化学神经递质的释放受神经末梢或末梢中细胞钙的短暂上升和衰减的调节。调节神经末梢中钙水平的任何物质都会反过来调节化学神经递质释放的速率、数量和持续时间。本研究的目的是以肾上腺嗜铬细胞为模型神经细胞系统，探讨神经递质释放的钙信号调节机制。嗜铬细胞来源于肾上腺内部，与神经相似，分泌神经激素肾上腺素和去甲肾上腺素，以响应细胞钙的升高。虽然调节细胞钙升高的细胞机制已经很好地理解，但调节用于分泌的钙信号的缓冲和衰减的那些机制还没有很好地定义。这些机制很重要，因为它们反过来会调节神经细胞之间通信的强度和持续时间。目前的项目将测试一种新的机制来调节钙信号衰减，该机制使用钠依赖性钙转运蛋白来从细胞中去除钙。这种转运蛋白被称为钠-钙交换剂，并且可以以几种不同的形式存在于不同的细胞区室中。钠-钙交换蛋白在钙信号衰减中的作用和性质将被确定。该项目将导致对调节神经递质释放的钙信号的细胞机制的更好理解，以及参与细胞钙清除和信号衰减的钙转运蛋白的识别。