LOCAL FIELD POTENTIALS IN THE BASAL GANGLIA

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 皮质输入到达基底节结构，基底节结构投射回丘脑和皮质。在帕金森病条件下，基底节出现同步振荡活动，这可以用局部场电位(LFP)记录来测量。 我们目前正在录制两只动物的照片。其中一只动物已经接受了大剂量的MPTP，并在几个月内缓慢给予，并患上了帕金森症，而另一只动物的MPTP治疗将很快开始(在正常状态下的研究完成后)。我们还检查了正常状态下注射多巴胺受体拮抗剂和帕金森病激动剂治疗的效果。我们发现，只有慢性多巴胺耗竭，而不是急性多巴胺受体阻断，才会产生显著的LFP变化。结合解剖学证据，这些发现表明慢性多巴胺丢失继发的形态变化对于振荡的改变是必要的。我们的结果表明，帕金森症状是明显的，没有LFP的变化，质疑病理振荡的致病作用。 彻底了解LFP变化和晚期帕金森病之间的关系也可能推动正在进行的将LFP信号用作帕金森患者按需深部脑刺激设备的控制信号的努力。在合作研究中，我们继续对人类患者进行这方面的探索。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Cortical inputs reach basal ganglia structures, which project back to thalamus and cortex. Under parkinsonian conditions, synchronized oscillatory activities appears in the basal ganglia which can be measured with local field potential (LFP) recordings. We are currently recording in two animals. One of them has received a large cumulative dose of MPTP, given slowly over several months, and has developed parkinsonism, while MPTP treatments in the other animal will start soon (after completion of studies in the normal state). We also examine effects of dopamine receptor antagonist injections in the normal state, and agonist treatment in parkinsonism. We found that only chronic dopamine depletion, but not acute dopamine receptor blockade, produces significant LFP changes. Together with anatomical evidence, these findings suggest that morphological changes secondary to chronic dopamine loss are necessary for changes in oscillations. Our results demonstrate that parkinsonism signs are manifest without LFP changes, questioning the causative role of pathological oscillations. A thorough understanding of the relationship between LFP changes and advanced parkinsonism may also advance ongoing efforts to use LFP signals as control signals for on-demand deep brain stimulation devices for parkinsonian patients. In collaborative studies, we have continued our exploration of this aspect in human patients