Investigating the role of sleep in synaptic reorganization after neural injury

研究睡眠在神经损伤后突触重组中的作用

基本信息

批准号：
10530705
负责人：
Jeffrey Michael Donlea
金额：
$ 39万
依托单位：
UNIVERSITY OF CALIFORNIA LOS ANGELES
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-12-01 至 2026-11-30
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10530705
关键词：
Acute Adult Astrocytes Axon Axotomy Back Biological Assay Brain Cell membrane Data Development Drosophila genus Drosophila melanogaster Endocytosis Excision Gene Expression Genes Genetic Injury Intervention Libraries Mediating Membrane Microglia Modeling Molecular Mushroom Bodies Mutation Nerve Nerve Degeneration Neurites Neuroglia Neuronal Injury Neuronal Plasticity Neurons Neuropeptides Neurophysiology - biologic function Neurotransmitters Olfactory Receptor Neurons Peptide Receptor Peptides Phagocytes Phagocytosis Process Proteins Public Health Recovery Regulator Genes Role Signal Transduction Sleep Sleep Deprivation Sleep disturbances Sleeplessness Synapses Synaptic plasticity Tachykinin Testing Trauma Wallerian Degeneration axon injury axonal degeneration cell type confocal imaging experimental study fly genetic regulatory protein injured insight memory encoding mutant nerve injury nerve transection neural neurochemistry neuromechanism neuroprotection presynaptic prevent programs receptor response response to injury sleep regulation synaptic pruning synthetic enzyme

项目摘要

Project Summary Sleep has been identified as a state of heightened neural plasticity, but the rules that govern reorganization during sleep remain unknown. To better identify the conditions under which synapses are pruned during sleep, we have begun to examine responses to neural injury in the fruit fly. After antennal transection, flies acutely increase their sleep for up to one day before returning back to baseline levels. Our preliminary data also show that pre-synaptic active zones are removed more rapidly than plasma membrane after antennal injury, and that sleep deprivation after injury prevents the clearance of pre-synapses from injured olfactory receptor neurons. In this project, we will examine: (1) signals that are generated after injuries to promote sleep; (2) contributions of glial cell types to sleep regulation and synapse removal after injury; and (3) molecular mechanisms that promote synapse removal during sleep. We anticipate that these experiments will provide insight into the role for sleep in response to neural trauma, and begin to investigate the consequences of disrupted sleep on recovery from axotomy.

项目摘要睡眠已被确定为神经可塑性增强的状态，但是控制重组的规则睡眠期间仍然未知。为了更好地确定睡眠期间突触的条件，我们已经开始研究果蝇中对神经损伤的反应。触角横断后，苍蝇急性在返回基线水平之前，将睡眠增加长达一天。我们的初步数据也显示触角损伤后，突触前的活性区比质膜更快地去除，并且受伤后的睡眠剥夺阻止了受伤的嗅觉受体神经元的同性恋的清除。在这个项目中，我们将研究：（1）受伤后产生的信号；（2）贡献受伤后的神经胶质细胞类型调节睡眠和突触去除；（3）分子机制在睡眠期间促进突触清除。我们预计这些实验将提供有关角色的洞察力响应神经创伤的睡眠，并开始研究睡眠破坏的后果从轴切开术中恢复。