Parr-Brownlie Louise C, Poloskey Stacey L, Bergstrom Debra A, Walters Judith R
Neurophysiological Pharmacology Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, 35 Convent Drive, Building 35 Room 1C 905, Bethesda, MD 20892-3702 USA.
Exp Neurol. 2009 Jun;217(2):269-81. doi: 10.1016/j.expneurol.2009.02.010. Epub 2009 Mar 5.
Parkinson's disease is associated with increased oscillatory firing patterns in basal ganglia output, which are thought to disrupt thalamocortical activity. However, it is unclear how specific thalamic nuclei are affected by these changes in basal ganglia activity. The thalamic parafascicular nucleus (PFN) receives input from basal ganglia output nuclei and directly projects to the subthalamic nucleus (STN), striatum and cortex; thus basal ganglia-mediated changes on PFN activity may further impact basal ganglia and cortical functions. To investigate the impact of increased oscillatory activity in basal ganglia output on PFN activity after dopamine cell lesion, PFN single-unit and local field potential activities were recorded in neurologically intact (control) rats and in both non-lesioned and dopamine lesioned hemispheres of unilateral 6-hydroxydopamine lesioned rats anesthetized with urethane. Firing rates were unchanged 1-2 weeks after lesion; however, significantly fewer spontaneously active PFN neurons were evident. Firing pattern assessments after lesion showed that a larger proportion of PFN spike trains had 0.3-2.5 Hz oscillatory activity and significantly fewer spike trains exhibited low threshold calcium spike (LTS) bursts. In paired recordings, more PFN-STN spike oscillations were significantly correlated, but as these oscillations were in-phase, results are inconsistent with feedforward control of PFN activity by inhibitory oscillatory basal ganglia output. Furthermore, the decreased incidence of LTS bursts is incompatible with inhibitory basal ganglia output inducing rebound bursting in PFN after dopamine lesion. Together, results show that robust oscillatory activity observed in basal ganglia output nuclei after dopamine cell lesion does not directly drive changes in PFN oscillatory activity.
帕金森病与基底神经节输出中振荡发放模式增加有关，这种模式被认为会扰乱丘脑皮质活动。然而，尚不清楚基底神经节活动的这些变化如何影响特定的丘脑核团。丘脑束旁核（PFN）接受来自基底神经节输出核的输入，并直接投射到丘脑底核（STN）、纹状体和皮质；因此，基底神经节介导的对PFN活动的改变可能会进一步影响基底神经节和皮质功能。为了研究多巴胺细胞损伤后基底神经节输出中振荡活动增加对PFN活动的影响，在神经功能完整的（对照）大鼠以及用乌拉坦麻醉的单侧6-羟基多巴胺损伤大鼠的未损伤和多巴胺损伤半球中记录了PFN单单位活动和局部场电位活动。损伤后1-2周放电率没有变化；然而，明显自发活动的PFN神经元数量显著减少。损伤后的发放模式评估表明，更大比例的PFN峰电位序列具有0.3-2.5Hz的振荡活动，并且表现出低阈值钙峰（LTS）爆发的峰电位序列显著减少。在配对记录中，更多的PFN-STN峰电位振荡显著相关，但由于这些振荡是同相的，结果与抑制性振荡基底神经节输出对PFN活动的前馈控制不一致。此外，LTS爆发发生率的降低与多巴胺损伤后抑制性基底神经节输出诱导PFN中的反弹爆发不相符。总之，结果表明多巴胺细胞损伤后在基底神经节输出核中观察到的强烈振荡活动不会直接驱动PFN振荡活动的变化。
