Takakusaki K, Obara K, Nozu T, Okumura T
Asahikawa Medical University, Midorigaoka-Higashi, Japan.
Arch Ital Biol. 2011 Dec;149(4):385-405. doi: 10.4449/aib.v149i4.1383. Epub 2011 Dec 1.
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.
脚桥被盖核（PPN）通过在清醒和快速眼动（REM）睡眠期间调节脑桥延髓网状脊髓系统的活动来参与控制肌张力。PPN接受来自黑质网状部（SNr）的GABA能投射，SNr是基底神经节的一个输出核。在此，我们研究了GABA能的SNr-PPN投射如何控制构成肌张力抑制系统的脑桥延髓网状脊髓束的活动。在去大脑猫（n = 14）的腰骶段对121个运动神经元进行了细胞内记录。向PPN施加短串刺激脉冲（3个脉冲，间隔5毫秒，10 - 40毫安），PPN中胆碱能神经元密集分布，刺激诱发向对侧方向的眼球运动，并双侧抑制伸肌活动。相同的PPN刺激在伸肌和屈肌运动神经元中诱发IPSPs，其峰值潜伏期为40 - 50毫秒，持续时间为40 - 50毫秒。晚期潜伏期的IPSPs由氯离子介导。向脑桥网状结构（PRF）微量注射硫酸阿托品（20毫摩尔，0.25毫升）可降低IPSPs的幅度。虽然单独施加于SNr的条件刺激（40 - 60毫安和100赫兹）未对运动神经元诱发任何突触后效应，但它降低了PPN诱发的IPSPs的幅度。随后向PPN注射荷包牡丹碱（5毫摩尔，0.25毫升）可阻断SNr的作用。向SNr微量注射NMDA（5毫摩尔，0.25毫升）和蝇蕈醇（5毫摩尔，0.25毫升）分别降低和增加了PPN诱发的IPSPs的幅度。这些结果表明，GABA能的基底神经节输出通过调节激活肌张力抑制系统的胆碱能PPN神经元的活动来控制姿势肌张力。SNr-PPN投射可能不仅有助于在清醒时运动期间控制肌张力，还参与REM睡眠期间肌肉张力缺失的调节。因此，SNr-PPN投射功能障碍可能与基底神经节疾病中的睡眠障碍有关。
