CORTICOTHALAMIC INPUT TO THE MOTOR THALAMUS

皮质丘脑对运动丘脑的输入

• 批准号: 7716378
• 负责人: MARJORIE E ANDERSON
• 金额: $ 15.78万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2009-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7716378
• 关键词: Animals; Attention; Behavioral; Calcium; Computer Retrieval of Information on Scientific Projects Database; Condition; Funding; Grant; Human; Impairment; Institution; Location; Modeling; Motor; Neurons; Parkinson Disease; Phase; Research; Research Personnel; Resources; Rotenone; Source; Thalamic structure; Toxin; Training; United States National Institutes of Health; disability

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Our objective is to determine the changes in discharge in the motor thalamus that occur in non-human models of Parkinson's disease, such as those induced by the toxins MPTP or rotenone, and the behavioral conditions under which these changes in discharge occur. Using the MPTP-induced model of Parkinson's disease, we have examined the burstiness of neurons in the thalamus during different phases (and different attention requirements) in a trained targeted reaching task and during different phases of MPTP-induced disability. The activity of over 500 thalamic neurons has been recorded during different behavioral states. If low-threshold calcium bursts (LTS) are identified and the percent of spikes in these bursts is determined, there is an increase in burstiness in severely impaired animals, but not so much in mild impairment. Further analysis, including the location of neurons with different degrees of burstiness and the different types of discharge irregularity and oscillations is under way.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 我们的目标是确定帕金森病非人类模型中运动丘脑放电的变化，例如由毒素 MPTP 或鱼藤酮诱导的放电变化，以及这些放电变化发生的行为条件。 使用 MPTP 诱导的帕金森病模型，我们检查了在经过训练的目标到达任务的不同阶段（和不同的注意力要求）以及 MPTP 诱导的残疾的不同阶段期间丘脑神经元的突发性。 超过 500 个丘脑神经元在不同行为状态下的活动已被记录。 如果识别出低阈值钙爆发 (LTS) 并确定这些爆发中峰值的百分比，则严重受损动物的爆发性会增加，但轻度受损动物的爆发性不会增加那么多。 进一步的分析正在进行中，包括不同程度的突发性神经元的位置以及不同类型的放电不规则性和振荡。