The Effect of Normal and Prolonged Sensory Activity on Neural Circuits
正常和长时间的感觉活动对神经回路的影响
基本信息
- 批准号:9261229
- 负责人:
- 金额:$ 2.47万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2014
- 资助国家:美国
- 起止时间:2014-02-01 至 2018-01-31
- 项目状态:已结题
- 来源:
- 关键词:Adaptive BehaviorsAddressAdultAffectAfferent NeuronsAnimal ModelAnimalsAutistic DisorderBasic ScienceBehaviorBehavioral AssayBenzaldehydeBinding ProteinsBrainCadherinsCaenorhabditis elegansCalciumCell Adhesion MoleculesCellsCellular biologyDefectDevelopmentEventG-Protein-Coupled ReceptorsGene ExpressionGenesGeneticGenetic ModelsGenetic ScreeningGoalsHealthHumanImageImageryIndividualLabelLifeMeasuresMediatingMessenger RNAMissionMolecularNational Institute of Neurological Disorders and StrokeNerve DegenerationNervous system structureNeuraxisNeuronsNucleotidesOdorsOrganismOutputPathway interactionsPerceptionPlayProcessProteinsReporterResearchResearch SupportResolutionRoleSchizophreniaSensorySignal PathwaySignal TransductionSignaling MoleculeStructureSynapsesSynaptic plasticitySystemTechniquesTestingTherapeuticTimeTransgenic OrganismsWorkbasebrain behaviorcell typecomplement C2acritical periodfluorophorefunctional plasticitygene discoverygenetic approachin vivoinnovationloss of functionmutantnervous system developmentnervous system disorderneural circuitneuroligin 1optogeneticspostsynapticreconstitutionresearch studyresponsesensory stimulussynaptic functiontool
项目摘要
DESCRIPTION (provided by applicant): The human central nervous system is composed of 100 billion neurons interconnected into precisely regulated circuits to mediate vital functions such as perception, thought, and behavior. Sensory activity has long been known to have important affects on synaptic plasticity. Understanding the molecular underpinnings of these processes may aid in understanding neurological disorders, such as autism and schizophrenia. However, much remains unknown about the molecular mechanisms by which normal activity and long-term activity affect synaptic plasticity. The discovery of molecules required in these pathways may be accelerated by the study of genetic model organisms, in which large-scale gene discovery techniques are feasible. To address this, we propose to take an innovative approach to studying the affects of sensory activity on synaptic plasticity, investigating all leves of the responses within two defined circuits in the genetic model organism C. elegans. We will assay behavioral output at the highest level, cellular-level calcium responses, specific synaptic connections between the neurons utilizing the trans-synaptic split-GFP based marker NLG-1 GRASP, and the individual molecules required for these events. This integrative proposal is relevant to the NINDS mission to support research that aims to reduce the burden of neurological disease by supporting basic research on the biology of the cells of the nervous system, nervous system development, genetics of the brain, behavior, neurodegeneration, brain plasticity, sensory function, synapses, and circuits. Using this approach, we have discovered a Galpha-olf-dependent pathway by which normal sensory activity maintains appropriate synaptic connections, and an EGL-4/PKG dependent pathway by which animals adapt to long-term sensory signaling. Our research will characterize the mechanism by which these pathways affect structural and functional synaptic plasticity. Our specific aims are to: 1) elucidate the molecular pathway by which normal sensory activity affects structural plasticity, and 2) determine the molecular basis for plasticity induced by long-term sensory activity. The robust prior characterization of these two circuits, in combination with the powerful tools we have available to study them, offers the unique potential to discover new and unexpected signaling pathways that mediate sensory activity dependent synaptic plasticity, which can then be explored in other systems.
描述(由申请人提供):人类中枢神经系统由1000亿个神经元组成,这些神经元相互连接成精确调节的回路,以调节感知、思维和行为等重要功能。长期以来,人们都知道感觉活动对突触可塑性有重要影响。了解这些过程的分子基础可能有助于理解神经系统疾病,如自闭症和精神分裂症。然而,关于正常活动和长时程活动影响突触可塑性的分子机制仍有许多未知之处。这些途径中所需分子的发现可能通过遗传模式生物的研究来加速,其中大规模基因发现技术是可行的。为了解决这个问题,我们建议采取一种创新的方法来研究感觉活动对突触可塑性的影响,在遗传模式生物C中的两个定义的回路内调查所有级别的响应。优雅的我们将分析最高水平的行为输出、细胞水平的钙反应、利用基于跨突触分裂GFP的标记物NLG-1 GRASP的神经元之间的特定突触连接以及这些事件所需的单个分子。这一综合性建议与NINDS的使命有关,即通过支持神经系统细胞生物学、神经系统发育、大脑遗传学、行为、神经变性、大脑可塑性、感觉功能、突触和电路的基础研究,支持旨在减轻神经系统疾病负担的研究。使用这种方法,我们已经发现了一个Galpha-olf依赖的途径,通过它正常的感觉活动保持适当的突触连接,和EGL-4/PKG依赖的途径,动物适应长期的感觉信号。我们的研究将描述这些通路影响结构和功能突触可塑性的机制。我们的具体目标是:1)阐明正常感觉活动影响结构可塑性的分子途径,2)确定长期感觉活动诱导的可塑性的分子基础。这两个电路的强大的先前表征,结合我们可以用来研究它们的强大工具,提供了发现新的和意想不到的信号通路的独特潜力,这些信号通路介导感觉活动依赖的突触可塑性,然后可以在其他系统中进行探索。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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{{ truncateString('Noelle D L 'Etoile', 18)}}的其他基金
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10739237 - 财政年份:2023
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
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- 批准号:
10201755 - 财政年份:2014
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The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
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10438733 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10657364 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Normal and Prolonged Sensory Activity on Neural Circuits
正常和长时间的感觉活动对神经回路的影响
- 批准号:
8686580 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10831919 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10002309 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10406068 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Normal and Prolonged Sensory Activity on Neural Circuits
正常和长时间的感觉活动对神经回路的影响
- 批准号:
8795234 - 财政年份:2014
- 资助金额:
$ 2.47万 - 项目类别:
The Effect of Sleep on Neural Circuit Connections
睡眠对神经回路连接的影响
- 批准号:
10444697 - 财政年份:2014
- 资助金额:
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