Pedunculopontine tegmental nucleus (PPN) contributes to the control muscle tone by modulating the activities of pontomedullary reticulospinal systems during wakefulness and rapid eye movement (REM) sleep. The PPN receives GABAergic projection from the substantia nigra pars reticulata (SNr), an output nucleus of the basal ganglia. Here we examined how GABAergic SNr-PPN projection controls the activity of the pontomedullary reticulospinal tract that constitutes muscle tone inhibitory system. Intracellular recording was made from 121 motoneurons in the lumbosacral segments in decerebrate cats (n=14). Short train pulses of stimuli (3 pulses with 5 ms intervals, 10-40 mA) applied to the PPN, where cholinergic neurons were densely distributed, evoked eye movements toward to the contralateral direction and bilaterally suppressed extensor muscle activities. The identical PPN stimulation induced IPSPs, which had a peak latency of 40-50 ms with a duration of 40-50 ms, in extensor and flexor motoneurons. The late-latency IPSPs were mediated by chloride ions. Microinjection of atropine sulfate (20 mM, 0.25 ml) into the pontine reticular formation (PRF) reduced the amplitude of the IPSPs. Although conditioning stimuli applied to the SNr (40-60 mA and 100 Hz) alone did not induce any postsynaptic effects on motoneurons, it reduced the amplitude of the PPN-induced IPSPs. Subsequent injection of bicuculline (5 mM, 0.25 ml) into the PPN blocked the SNr effects. Microinjections of NMDA (5 mM, 0.25 ml) and muscimol (5 mM, 0.25 ml) into the SNr reduced and increased the amplitude of the PPN-induced IPSPs, respectively. These results suggest that GABAergic basal ganglia output controls postural muscle tone by modulating the activity of cholinergic PPN neurons which activate the muscle tone inhibitory system. The SNr-PPN projection may contribute to not only control of muscle tone during movements in wakefulness but also modulation of muscular atonia of REM sleep. Dysfunction of the SNr-PPN projection may therefore be involved in sleep disturbances in basal ganglia disorders.

中文翻译：

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GABA能性基底节神经元神经元对猫的PPN和肌张力抑制系统的调节作用。

枕形枕骨被膜核（PPN）通过在清醒和快速眼动（REM）睡眠期间调节桥突网状脊椎系统的活动，从而有助于控制肌张力。PPN接收来自黑质网状体（SNr）（基底神经节的输出核）的GABA能投影。在这里，我们检查了GABA能级SNr-PPN投射如何控制构成肌肉张力抑制系统的桥突网状脊髓束的活动。在小脑猫（n = 14）的腰s部中的121个运动神经元进行细胞内记录。在PPN上施加短时间的刺激刺激脉冲（3个脉冲，间隔5 ms，10-40 mA），胆碱能神经元密集分布，引起眼球朝对侧方向运动，并双侧抑制伸肌活动。在伸肌和屈肌运动神经元中，相同的PPN刺激诱导IPSPs的潜伏期为40-50 ms，持续时间为40-50 ms。延迟潜伏期IPSP是由氯离子介导的。将硫酸阿托品（20 mM，0.25 ml）微量注射到脑桥网状结构（PRF）中可降低IPSP的振幅。尽管仅对SNr（40-60 mA和100​​ Hz）施加条件刺激不会对运动神经元产生任何突触后影响，但它会降低PPN诱导的IPSP的幅度。随后向PPN中注射双小分子（5 mM，0.25 ml）阻止了SNr效应。微量注射NMDA（5 mM，0.25 ml）和muscimol（5 mM，0。进入SNr（25 ml）会分别降低和增加PPN诱导的IPSP的幅度。这些结果表明，GABA能基神经节输出通过调节胆碱能PPN神经元的活性来控制姿势肌张力，从而激活肌张力抑制系统。SNr-PPN投影不仅有助于控制清醒运动过程中的肌肉张力，而且还有助于调节REM睡眠的肌肉无力状态。因此，SNr-PPN投影功能障碍可能与基底神经节疾病的睡眠障碍有关。SNr-PPN投影不仅有助于控制清醒运动过程中的肌肉张力，而且还有助于调节REM睡眠的肌肉无力状态。因此，SNr-PPN投影功能障碍可能与基底神经节疾病的睡眠障碍有关。SNr-PPN投影不仅有助于控制清醒运动过程中的肌肉张力，而且还有助于调节REM睡眠的肌肉无力状态。因此，SNr-PPN投影功能障碍可能与基底神经节疾病的睡眠障碍有关。