Calcium channels in retinal photoreceptors

视网膜感光器中的钙通道

基本信息

批准号：
9238359
负责人：
Sheila A Baker
金额：
$ 56.86万
依托单位：
UNIVERSITY OF IOWA
依托单位国家：
美国
项目类别：
财政年份：
2017
资助国家：
美国
起止时间：
2017-03-01 至 2022-02-28
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9238359
关键词：
3-Dimensional Affect Aging Binding Biochemical Biological Blindness Brain Calcium Channel Cell Count Cell Transplantation Cell surface Cells Characteristics Communication Cone Defect Dendrites Development Disease Electron Microscopy Electrophysiology (science)Electroporation Functional disorder Genetic Glutamates Goals Heart Image Inherited Injury Knock-out Knockout Mice Knowledge Mediating Membrane Metabotropic Glutamate Receptors Microscopy Modeling Mus Mutation Night Blindness Organelles Outcomes Research Photoreceptors Presynaptic Terminals Process Property Proteins Proteomics Research Priority Resolution Retina Retinal Detachment Retinal Diseases Retinal Photoreceptors Retinitis Pigmentosa Role Signal Transduction Synapses Techniques Testing Vertebrate Photoreceptors Vision Vision Disorders Visual Work extracellular in vivo mutant neurotransmission neurotransmitter release novel novel strategies novel therapeutics optical imaging postsynaptic presynaptic prevent restoration retinal rods ribbon synapse scaffold synaptic function synaptogenesis voltage

项目摘要

Communication at the first visual synapse is mediated by L-type voltage-gated Cav1.4 Ca2+ channels. These channels are concentrated in the synaptic terminal beneath the ribbon, an organelle characteristic of synapses employing tonic neurotransmitter release. Mutation of Cav1.4 alters neurotransmission but can also prevent synaptic development. Such defects can present as a variety of visual diseases, including congenital stationary night blindness or cone-rod dystrophy. In this proposal, we will test the hypothesis that Cav1.4 (Aim 1) and its auxiliary subunits, β2 (Aim 2) and α2δ4 (Aim 3), are each essential in various ways for synaptic development in photoreceptors. This work will be accomplished using a complementary array of electrophysiological, genetic, biochemical, and cell biological approaches. The outcomes of this research should have a broad impact by transforming the concept of how Cav1.4 channels contribute to synapse function and disease-triggered remodeling.

第一个视觉突触的通讯由 L 型电压门控 Cav1.4 Ca2+ 介导这些通道集中在带状体下方的突触末端。采用强直性神经递质释放的突触特征的细胞器。 Cav1.4 会改变神经传递，但也会阻止突触发育。表现为多种视觉疾病，包括先天性静止性夜盲症或视杆细胞营养不良。在本提案中，我们将检验 Cav1.4（目标 1）及其辅助假设。亚基 β2（目标 2）和 α2δ4（目标 3）在不同方面对于突触至关重要这项工作将使用一系列互补的技术来完成。电生理学、遗传学、生物化学和细胞生物学方法的结果。通过改变 Cav1.4 通道的概念，研究应该会产生广泛的影响有助于突触功能和疾病触发的重塑。