Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat

Unilateral lesion of the nigrostriatal pathway induces an increase of neuronal activity of the pedunculopontine nucleus, which is reversed by the lesion of the subthalamic nucleus in the rat
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DOI:
10.1046/j.0953-816x.2001.01800.x
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发表时间:
2001-12-01
影响因子:
3.4
通讯作者:
Benazzouz, A
Benazzouz, A
中科院分区:
医学3区
文献类型:
--
作者:
Breit, S;Bouali-Benazzouz, R;Benazzouz, A

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桥小脑脚核(PPN)在帕金森病的病理生理学中的作用尚不清楚。我们用显微记录技术研究了损毁黑质致密区(SNC)后PPN神经元的变化以及丘脑底核(STN)在这些变化中的作用。正常大鼠PPN神经元的放电频率为10.6+/-1.4个/S,多数神经元(91%)具有规则的放电模式,6%为不规则放电模式,3%为阵发性放电模式。损毁6-羟基多巴胺的黑质大鼠,放电频率较正常大鼠显著增加,达18.3+/-3.0个/S。此外,放电模式发生了显著变化:70%的神经元规则放电,27%的神经元不规则放电,3%的神经元呈阵发性放电。在鹅膏毒素损毁STN的大鼠,放电频率显著降低至7.2+/-0.9个/S,放电模式发生明显改变:50%的神经元规则放电,43%的神经元不规则放电,7%的神经元爆发。SNc和STN联合损毁大鼠的放电频率(8.5+/-1.0锋/S)与正常大鼠相比无明显变化。放电模式发生了显著变化:69%的细胞规则放电,26%的细胞不规则放电,5%的细胞呈阵发性放电。这些结果表明,在6-羟基多巴胺损毁的大鼠,PPN神经元过度活跃且更加不规则,提示该核团在帕金森病的病理生理学中的意义。此外,损毁STN导致正常大鼠PPN放电频率降低,6-羟基多巴胺损毁大鼠PPN放电频率正常化,表明该核团主要受控于STN。
The role of the pedunculopontine nucleus (PPN) in the pathophysiology of Parkinson's disease is still unclear. Using microrecordings, we investigated the changes occurring in PPN neurons after lesions of the substantia nigra compacta (SNc) and the role of the subthalamic nucleus (STN) in these changes. In normal rats the firing rate of PPN neurons was 10.6 +/- 1.4 spikes/s, the majority of neurons (91%) having a regular firing pattern, 6% irregular and 3% in bursts. In rats with 6-hydroxydopamine lesions of the SNc, the firing rate increased significantly to 18.3 +/- 3.0 spikes/s compared with normal rats. In addition, the firing pattern changed significantly: 70% of the neurons discharged regularly, 27% irregularly and 3% in bursts. In rats with ibotenic acid lesions of the STN, the firing rate decreased significantly to 7.2 +/- 0.9 spikes/s and the firing pattern changed significantly: 50% of the neurons discharged regularly, 43% irregularly and 7% in bursts. The rats with combined SNc and STN lesions showed no change in the firing rate (8.5 +/- 1.0 spikes/s) compared to normal rats. The firing pattern changed significantly: 69% of the cells discharged regularly, 26% irregularly and 5% in bursts. These findings demonstrate that PPN neurons are overactive and more irregular in the 6-hydroxydopamine-lesioned rats, suggesting the implication of this nucleus in the pathophysiology of parkinsonism. Moreover, the fact that STN lesions induced a reduction in the firing rate of the PPN in normal rats and a normalization of the firing rate in rats with 6-hydroxydopamine lesions suggests that this nucleus is under major control of the STN.