LOCAL FIELD POTENTIALS IN THE BASAL GANGLIA

这个子项目是许多利用资源的研究子项目之一 由NIH/NCRR资助的中心拨款提供。子项目的主要支持 而子项目的主要调查员可能是由其他来源提供的， 包括其它NIH来源。 列出的子项目总成本可能 代表子项目使用的中心基础设施的估计数量， 而不是由NCRR赠款提供给子项目或子项目工作人员的直接资金。 皮质输入到达基底神经节结构，其投射回丘脑和皮质。在帕金森病条件下，同步振荡活动出现在基底神经节，这可以用局部场电位（LFP）记录来测量。 我们目前正在记录两只动物。 其中一只动物接受了大剂量的MPTP累积治疗，在几个月内缓慢给予，并出现了帕金森症，而另一只动物的MPTP治疗将很快开始（在正常状态下完成研究后）。 我们还研究了多巴胺受体拮抗剂注射在正常状态下的作用，以及帕金森症的激动剂治疗。 我们发现，只有慢性多巴胺耗竭，而不是急性多巴胺受体阻滞，产生显着的LFP的变化。 结合解剖学证据，这些发现表明，继发于慢性多巴胺丢失的形态学变化是振荡变化所必需的。 我们的研究结果表明，帕金森氏症的迹象是明显的LFP的变化，质疑病理振荡的致病作用。 对LFP变化与晚期帕金森症之间关系的深入了解也可能推动将LFP信号用作帕金森病患者按需脑深部电刺激设备的控制信号的持续努力。 在合作研究中，我们继续在人类患者中探索这方面的问题

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