权益分类	功能权益	普通用户	{{item.name}}会员
{{category.name}}	{{benefitItem.name}}

Connexin 43 Modulates Regulated Exocytosis

连接蛋白 43 调节胞吐作用

基本信息

批准号：
10164801
负责人：
VLADIMIR PARPURA
金额：
$ 33.41万
依托单位：
UNIVERSITY OF ALABAMA AT BIRMINGHAM
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-09-01 至 2023-05-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10164801
关键词：
Address Affect Affinity Chromatography Agonist Alzheimer&apos s Disease Astrocytes Binding Sites Biology Bradykinin Brain Brain Diseases Cell Culture Techniques Cell membrane Cells Clathrin Communication Conflict (Psychology)Connexin 43 Connexins Coupled Data Deletion Mutation Disease Endocytosis Ensure Exocytosis Fluorescence Microscopy Gap Junctions Glutamate Receptor Glutamates Health High Pressure Liquid Chromatography Image Infection Intervention Investigation Ischemia Knock-out Laboratories Learning Life Link Literature Location Mediating Memory Microscopy Microtubule Proteins Microtubule Stabilization Microtubules Molecular Molecular Target Multiple Sclerosis Mutation Neurons Osteoblasts PHluorin Pharmacology Process Proteins Proteomics Reproducibility Resolution Respiration Retrieval Role Secretory Vesicles Seizures Signal Transduction Site Slice Stroke Structural Protein Synapses Synaptic Transmission Techniques Testing Traumatic Brain Injury Tubulin VAMP-2 Vesicle Work bone cell type depolymerization designer receptors exclusively activated by designer drugs experimental study insight interest novel sleep regulation subcellular targeting tandem mass spectrometry vesicular release virtual

项目摘要

Abstract Astrocyte-neuron signaling, a.k.a. gliotransmission, can modulate synaptic transmission/plasticity at tripartite synapses. Among the processes regulated by gliotransmission are sleep-regulation, respiration, and learning/memory. Despite these roles of gliotransmission in such fundamental life processes, its mechanism is not understood. Elucidating this mechanism should provide insights into basic brain processes, and suggest interventions when they go awry. Two early studies of astrocyte-neuron signaling explored the hypothesis that astrocytic glutamate release acts on neuronal glutamate receptors, but they led to different conclusions regarding the mechanism. One study concluded that glutamate is not the messenger but instead suggested that gap junctions might mediate astrocyte-neuron signaling. The other study concluded that the signaling is mediated by Ca2+-dependent glutamate release from astrocytes, subsequently shown to occur by regulated exocytosis of glutamate-containing vesicles. Virtually nothing is known about the subcellular distribution/localization of astrocyte release sites. It is not clear if they are localized uniquely to the tripartite synaptic regions of astrocytes or more broadly. There is much debate about the relative roles of exocytosis vs. gap junction-mediated communication as critical for astrocyte-neuron signals. Our preliminary data point to a novel, unifying hypothesis that these two mechanisms are, in fact, mechanistically linked.

摘要