Calcium signaling in retinal glia

视网膜神经胶质细胞中的钙信号传导

• 批准号: 121657-2008
• 负责人: Kelly, Melanie
• 金额: $ 3.34万
• 依托单位: Dalhousie University
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2009
• 资助国家: 加拿大
• 起止时间: 2009-01-01 至 2010-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=422016
• 关键词: Calcium; signaling; retinal; glia

The retina is a thin layer of transparent tissue made up of neurons and non-neural cells that are responsible for converting visual images into electrical signals. These electrical signals are transmitted to the brain via the optic nerve and result in our visual perception. The primary non-neural cells in the retina are glial cells. There are two different types of glial cells in the retina: Müller glia and astrocytes. Müller glia are the principal glial cell type in the vertebrate retina and are radial glia that span three synaptic layers. Müller glia provide important homeostatic functions, including neurotransmitter uptake and buffering of ions released during neuronal activity. In addition, Müller glia also directly participate with neurons in bidirectional communication. They do this by responding to released neurotransmitters and, in turn, releasing glial transmitters and neuroactive molecules that can have effects on retinal neurons and vasculature. Receptor-activated calcium increases are key to the response of these cells to neurotransmitters and to the subsequent release of glial transmitters. Increases in calcium in Müller glia involve calcium release from intracellular stores and calcium entry across the cell membrane. Alterations in Müller glia calcium signaling are associated with gliosis, a condition in which quiescent Müller glia in the postnatal retina proliferate in response to injury. Our research is examining the cellular pathways, specifically calcium entry channels, involved in receptor-activated calcium increases in Müller glia and the relationship between glial calcium signals and cell proliferation. These studies will provide new knowledge about glial cell signaling in the retina and are fundamental for understanding the role of glial cells in retinal physiology and pathophysiology.

视网膜是由神经元和非神经细胞组成的透明组织薄层，负责将视觉图像转换为电信号。这些电信号通过视神经传输到大脑，并导致我们的视觉感知。视网膜中的主要非神经细胞是神经胶质细胞。视网膜中有两种不同类型的神经胶质细胞：Müller神经胶质细胞和星形胶质细胞。米勒神经胶质是脊椎动物视网膜中的主要神经胶质细胞类型，并且是跨越三个突触层的放射状神经胶质。Müller胶质细胞提供重要的稳态功能，包括神经递质摄取和缓冲神经元活动期间释放的离子。此外，Müller胶质细胞还直接参与与神经元的双向通讯。它们通过对释放的神经递质做出反应来做到这一点，反过来，释放神经胶质递质和神经活性分子，这些分子可以对视网膜神经元和血管系统产生影响。受体激活的钙增加是这些细胞对神经递质的反应和随后释放神经胶质递质的关键。Müller胶质细胞中钙的增加涉及钙从细胞内储存释放和钙穿过细胞膜进入。Müller神经胶质钙信号的改变与神经胶质增生有关，神经胶质增生是一种出生后视网膜中静止的Müller神经胶质对损伤的反应。我们的研究是检查细胞通路，特别是钙离子进入通道，参与受体激活的钙离子在Müller神经胶质细胞的增加和神经胶质细胞的钙信号和细胞增殖之间的关系。这些研究将提供有关视网膜中神经胶质细胞信号传导的新知识，并且是理解神经胶质细胞在视网膜生理学和病理生理学中的作用的基础。