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Regulation of Retinal Gap Junctions

视网膜间隙连接的调节

基本信息

批准号：
8244508
负责人：
JOHN O'BRIEN
金额：
$ 36万
依托单位：
UNIVERSITY OF TEXAS HLTH SCI CTR HOUSTON
依托单位国家：
美国
项目类别：
财政年份：
2000
资助国家：
美国
起止时间：
2000-02-01 至 2014-03-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8244508
关键词：
Adenosine Affect Amacrine Cells Binding Biological Models Biological Neural Networks C-terminal Cell Communication Cell Culture System Cell Culture Techniques Cells Complex Connexins Coupled Coupling Cyclic AMP Cyclic AMP-Dependent Protein Kinases Data Degenerative Disorder Dependence Disease Dopamine Dopamine D1 Receptor Elements Epilepsy Equilibrium Gap Junctions Glutamates Goals Intervention Lead Light Light Adaptations Link Macular degeneration Maintenance Mammals Mediating Memory Molecular Motor Mutagenesis Neuraxis Neurons Oryctolagus cuniculus PDZ protein Pattern Phosphoric Monoester Hydrolases Phosphorylation Photoreceptors Plastics Play Process Property Protein Binding Protein Dephosphorylation Protein Isoforms Protein Kinase Protein Phosphatase 2A Regulatory Subunit PR53 Protein phosphatase Proteins Receptor Activation Regulation Research Retina Retinal Retinal Degeneration Role Second Messenger Systems Signal Pathway Signal Transduction Site Small Interfering RNA Study models Synapses System Testing Time Tracer Vision Disorders Visual Acuity Zebrafish cell type computerized data processing connexin 36 density genetic regulatory protein hearing impairment killings neural circuit receptive field receptor research study response retinal neuron retinal rods second messenger visual adaptation

项目摘要

Electrical coupling mediated by gap junctions contributes to the signal processing functions of most types of retinal neurons. Modulation of gap junctions during visual adaptation has profound effects on sensitivity and receptive field properties of many neurons and influences the path of signal flow in the mammalian rod circuit. The long-term objectives of this study are to identify the mechanisms that regulate electrical coupling in the retina, and to determine which modes of regulation are most important for the adaptive processes observed in different electrically coupled neural circuits. Previous results have indicated that phosphorylation of gap junction proteins is a critical mechanism to regulate coupling. Phosphorylation of connexin 35/36 (Cx35/36) gap junctions changes dynamically with light adaptation and correlates directly with coupling. In this project, we will examine the profoundly different signaling mechanisms that control coupling through Cx35/36 gap junctions in AII amacrine cells and photoreceptors. We will identify the key molecular components that couple and uncouple the gap junctions in these two systems, and examine the factors that contribute to the assembly of these different signaling modules. This research will shed light on the fundamental mechanisms that control electrical coupling, and reveal signaling pathways that may be defective in visual disorders.

由间隙连接介导的电耦合有助于大多数类型的神经元的信号处理功能。视网膜神经元在视觉适应过程中缝隙连接的调节对敏感性和许多神经元的感受野特性，并影响哺乳动物杆回路中的信号流路径。这项研究的长期目标是确定调节电耦合的机制，视网膜，并确定哪些调节模式是最重要的适应性过程中观察到的，不同的电耦合神经回路以前的研究结果表明，磷酸化的差距，连接蛋白是调节偶联的关键机制。连接蛋白35/36（Cx 35/36）的磷酸化间隙连接随光适应而动态变化，并与耦合直接相关。在本项目中，我们将研究通过Cx 35/36间隙控制偶联的完全不同的信号传导机制 AII无长突细胞和光感受器的连接。我们将找出关键的分子组成部分，并将这两个系统中的差距连接分开，并检查有助于组装的因素这些不同的信号模块。这项研究将揭示控制这种疾病的基本机制，电耦合，并揭示信号通路，可能是有缺陷的视觉障碍。