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Arousal and Timekeeping in a Mouse Model of Parkinsonism

帕金森病小鼠模型的唤醒和计时

基本信息

批准号：
10437525
负责人：
CATALIN V. BUHUSI
金额：
$ 43.8万
依托单位：
UTAH STATE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2022
资助国家：
美国
起止时间：
2022-04-01 至 2025-03-31
项目状态：
未结题

来源：
https://reporter.nih.gov/project-details/10437525
关键词：
Aging Agonist Alzheimer&apos s Disease Animal Model Arousal Attention Behavior Behavioral Behavioral Genetics Biochemical C57BL/6 Mouse Clinical Treatment Cognition Cognitive Cognitive deficits Corpus striatum structure Decision Making Diurnal Rhythm Dopamine Emotional Executive Dysfunction Generations Goals Huntington Disease Hypothalamic structure Impaired cognition Impairment Infusion procedures Lateral Lesion Medial Mental Depression Methods Modeling Motor Motor Activity Movement Movement Disorders Mus Nerve Degeneration Neurons Neurotransmitters Norepinephrine Outcome Parkinson Disease Parkinsonian Disorders Pathway interactions Patients Performance Pharmaceutical Preparations Pharmacology Prefrontal Cortex Process Production Protocols documentation Reproduction Response to stimulus physiology Role Sleep Symptoms Time Wakefulness alertness behavioral response classical conditioning cognitive control cognitive enhancement cognitive function cognitive performance executive function frontal lobe glial cell-line derived neurotrophic factor hypocretin improved locus ceruleus structure migration motivated behavior motor control motor deficit motor impairment mouse model neural circuit neurobiological mechanism neuronal circuitry neuropsychiatric disorder noradrenergic novel object recognition receptor response sensory input shift work stem treatment strategy vigilance way finding

项目摘要

PROJECT SUMMARY / ABSTRACT Movement disorders, such as Parkinson’s Disease (PD) and Huntington’s Disease, are characterized by drastic impairments in planning and executing movement, as well as cognitive deficits, some of which stem from deficits in estimating durations. Estimation and reproduction of durations in the seconds-to-minutes range are critical for fundamental processes such as associative learning, planned motor responses and decision-making. This project will explore neurobiological mechanisms involved in the estimation and reproduction of durations to evaluate timed motor response deficits in mouse models of PD. We will investigate the role of arousal, and the involvement of a novel neurotransmitter, orexin, in alterations of timed response selection using a newly developed model of timed response selection deficits in PD. We will also evaluate pharmacological approaches to rescue motor timing deficits. The project will enhance our understanding of neuronal processes involved in cognitive and motor control deficits in movement disorders, and will help develop new treatment strategies in animal models, with possible subsequent impact on clinical treatments.

项目总结/摘要运动障碍，如帕金森病（PD）和亨廷顿病，是以计划和执行运动以及认知能力的严重受损为特征，赤字，其中一些源于赤字估计持续时间。估计和复制持续时间在秒到分钟的范围内，对于基本过程至关重要，联想学习、有计划的运动反应和决策。该项目将探索神经生物学机制参与估计和再现的持续时间，评估PD小鼠模型中的定时运动反应缺陷。我们将研究唤醒，以及一种新的神经递质，食欲素的参与，在时间的改变，反应选择使用新开发的模型的定时反应选择赤字在PD。我们还将评估挽救运动计时缺陷的药理学方法。项目将增强我们对参与认知和运动控制的神经元过程的理解运动障碍的缺陷，并将有助于开发新的治疗策略，在动物模型，可能对临床治疗产生后续影响。