Neuronal ensembles of compulsive alcohol drinking
Neuronal ensembles of compulsive alcohol drinking
批准号:
10224712
负责人:
Olivier George
金额:
$35.55万
依托单位国家:
美国
项目类别:
财政年份:
2017
资助国家:
美国
项目状态:
已结题
起止时间:
2017-08-01 至 2022-07-31
关键词:
AcuteAddressAlcohol consumptionAlcohol dependenceAlcoholsAmygdaloid structureBehavior ControlBrainBrain regionCell NucleusChronicCorticotropin-Releasing HormoneDevelopmentEventFOS geneHeavy DrinkingHyperalgesiaHypothalamic structureImmediate-Early GenesInvestigationKnowledgeLacZ GenesLateralLeadLiteratureMediatingMethodsMotivationNeurobiologyNeuronsPainPathway interactionsPharmacogeneticsPharmacologyPhenotypePopulationRattusRoleSaccharinSelf AdministrationStructure of terminal stria nuclei of preoptic regionTechniquesTestingTimeTransgenic OrganismsWithdrawalalcohol exposureanxiety-like behaviordesignexperimental studyimprovednegative emotional stateneurobiological mechanismneuronal circuitrynoveloptogeneticsparabrachial nucleuspreventrecruittoolvapor
中文摘要
项目摘要/摘要:
中国酒类领域面临的一个关键问题是,人们对他们所说的那些谨慎的神经元组缺乏足够的知识。
对酒精依赖患者的过度饮酒行为负有责任。这一问题是影响健康的一大主要障碍。
酒精领域之所以受到关注,是因为对全球神经元组的调查表明,可能会调解过度饮酒和饮酒行为。
为我们提供一个全面的、全面的、对导致酒精中毒的神经元回路的理解。
依赖性。这是最近药物遗传学技术和光遗传技术工具的最新发展趋势,这些工具将允许选择性药物靶向治疗。
这是一个巨大的机遇,可以弥合中国文献中的这一差距。-中国中央电视台
这一提议的假设是,臂旁核(PBN)和大脑中脑中央核团(PBN)的激活。
杏仁核(CEA)在戒断过程中负责管理一系列谨慎的神经系统整体的招募工作。
这些信息散布在整个大脑中,最终是过度饮酒的原因,并导致了糖尿病的出现。
消极的情绪障碍状态发生在依赖的老鼠身上。我们已经获得了一个强有力的初步研究结果,这表明这是有选择性的。
针对这些神经元群,可以产生一种持久的逆转依赖患者过度饮酒和饮酒习惯的效果。
老鼠,他们发现了这三个群体之间的因果关系,它们揭示了一种新的神经元传导途径。
有助于减少酒精依赖。一个具体的目标是第一个目标,这是美国CEA和中国PBN退出的主要作用。
神经元细胞系在过度饮酒和饮酒依赖的大鼠中发生的。这一特定的研究目标2剖析了该模型的主要作用。
不同的CEA和CRF途径参与了新的神经元群的招募工作,并纠正了过度饮酒和饮酒问题。
酗酒与依赖。这些研究的结果表明,酒精对青少年的潜在影响具有强大的影响力和持久的影响。
这是因为我们的研究方法将不会提高我们对酒精的主要神经生物学机制的理解。
依赖理论和方法确定了一种新的神经元群结构和回路结构,这些结构专门控制与之相关的行为。
酗酒和依赖。
英文摘要
Project Summary/Abstract
A key issue in the alcohol field is the lack of knowledge on the discreet neuronal ensembles that are
responsible for excessive alcohol drinking in alcohol-dependent subjects. This is a major obstacle for the
alcohol field because investigations of the neuronal ensembles that mediate excessive alcohol drinking would
provide a comprehensive understanding of the neuronal circuits that causally contribute to alcohol
dependence. The recent development of pharmacogenetic and optogenetic tools that allow selective targeting
of specific neuronal ensembles is a tremendous opportunity to bridge this gap in the literature. The central
hypothesis of this proposal is that activation of the parabrachial nucleus (PBN) and central nucleus of the
amygdala (CeA) during withdrawal is responsible for the recruitment of a set of discreet neuronal ensembles
that are scattered throughout the brain and ultimately responsible for excessive drinking and the emergence of
negative emotional states in dependent rats. We obtained robust preliminary results that show that selectively
targeting these neuronal ensembles produces long-lasting reversal of excessive alcohol drinking in dependent
rats, identifies a causal relationship between these ensembles, and reveals novel neuronal pathways that
contribute to alcohol dependence. Specific Aim 1 characterizes the role of the CeA and PBN withdrawal
neuronal ensembles in excessive alcohol drinking in dependent rats. Specific Aim 2 dissects the role of the
different CeA CRF pathways in the recruitment of the neuronal ensembles and excessive alcohol drinking in
alcohol dependence. Results from these studies have the potential to have a strong and lasting impact in the
field because our approach will improve our understanding of the neurobiological mechanisms of alcohol
dependence and identify novel neuronal populations and circuits that specifically control behaviors associated
with alcohol dependence.
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