Scarnati E, Di Loreto S, Proia A, Gallié G
Department of Biomedical Technology and Biometry, School of Medicine, University of L'Aquila, Italy.
Arch Ital Biol. 1988 Jun;126(3):145-63.
The purpose of this study was to investigate the influence of the pedunculopontine nucleus (PPN) on the electrical activity of entopeduncular nucleus (EP) in the rat and to analyze the influence of the subthalamic nucleus (STN) on the PPN-evoked responses of EP cells. Most of the EP neurons recorded (65.1%) were identified electrophysiologically as output cells projecting to the lateral habenula while only a minority (3.8%) were output cells to the PPN. Stimulation of the PPN in intact rats caused a short-latency (2.5 +/- 2.0, S.D. ms) activation in 22.6% and suppression of activity in 8.5% of EP neurons recorded. The mean impulse rate of EP neurons in intact rats was 27.0 +/- 5.5, S.D. imp./s and the overall mean interspike interval 36.8 +/- 7.1, S.D. ms. In rats where the PPN had been destroyed 10-12 days before recording by a local microinjection of kainic acid only a few EP neurons were still responsive to stimulation of the PPN showing suppression of activity. In these rats the kainate lesion slowed the impulse spontaneous activity to 14.3 +/- 6.3, S.D. imp./s and markedly altered the distribution of interspike intervals in 62.5% of the EP neurons recorded. The overall mean interspike interval in this group of deregulated neurons was 68.2 +/- 20.1, S.D. ms. A small kainate lesion of the STN placed 4-5 days before recording, on the other hand, did not affect the spontaneous activity of EP cells but increased the percentage of cells which were activated (43.6%) by stimulating the PPN. The present data demonstrate a predominant activatory influence of the PPN on EP cells and suggest that destruction of the STN may affect the responsiveness of entopeduncular cells to stimulation of the PPN possibly through the removal of a tonic inhibitory STN influence on the EP.
本研究的目的是探讨脚桥核（PPN）对大鼠内苍白球核（EP）电活动的影响，并分析丘脑底核（STN）对PPN诱发的EP细胞反应的影响。记录到的大多数EP神经元（65.1%）经电生理鉴定为投射至外侧缰核的输出细胞，而仅有少数（3.8%）是投射至PPN的输出细胞。在完整大鼠中刺激PPN，可使记录到的22.6%的EP神经元产生短潜伏期（2.5±2.0，标准差，毫秒）激活，8.5%的神经元活动受到抑制。完整大鼠中EP神经元的平均冲动频率为27.0±5.5，标准差，冲动/秒，总的平均峰峰间期为36.8±7.1，标准差，毫秒。在记录前10 - 12天通过局部微量注射 kainic 酸破坏PPN的大鼠中，仅有少数EP神经元仍对PPN刺激有反应，表现为活动受抑制。在这些大鼠中，kainate 损伤使冲动自发活动减慢至14.3±6.3，标准差，冲动/秒，并使62.5%记录到的EP神经元的峰峰间期分布发生显著改变。这组调节失调神经元的总的平均峰峰间期为68.2±20.1，标准差，毫秒。另一方面，在记录前4 - 5天对STN进行小的kainate损伤，并不影响EP细胞的自发活动，但增加了通过刺激PPN而被激活的细胞百分比（43.6%）。目前的数据表明PPN对EP细胞具有主要的激活作用，并提示破坏STN可能通过消除STN对EP的紧张性抑制作用，影响内苍白球细胞对PPN刺激的反应性。
