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刺激猫脑桥被盖脚桥核诱发肌肉弛缓时后肢运动神经元兴奋性的变化

Changes in the excitability of hindlimb motoneurons during muscular atonia induced by stimulating the pedunculopontine tegmental nucleus in cats.

作者信息

Takakusaki K, Habaguchi T, Saitoh K, Kohyama J

机构信息

Department of Physiology II, College of Medicine, Asahikawa Medical College, Midorigaoka Higashi 2-1, Asahikawa 078-8510, Japan.

出版信息

Neuroscience. 2004;124(2):467-80. doi: 10.1016/j.neuroscience.2003.12.016.

Abstract

We have previously reported that electrical stimulation delivered to the ventral part of the pedunculopontine tegmental nucleus (PPN) produced postural atonia in acutely decerebrated cats [Neuroscience 119 (2003) 293]. The present study was designed to elucidate synaptic mechanisms acting on motoneurons during postural atonia induced by PPN stimulation. Intracellular recording was performed from 72 hindlimb motoneurons innervating extensor and flexor muscles, and the changes in excitability of the motoneurons following the PPN stimulation were examined. Repetitive electrical stimulation (20-50 microA, 50 Hz, 5-10 s) of the PPN hyperpolarized the membrane potentials of both the extensor and flexor motoneurons by 2.0-12 mV (6.0 +/- 2.3 mV, n = 72). The membrane hyperpolarization persisted for 10-20 s even after termination of the stimulation. During the PPN stimulation, the membrane hyperpolarization was associated with decreases in the firing capability (n = 28) and input resistance (28.5 +/- 6.7%, n = 14) of the motoneurons. Moreover the amplitude of Ia excitatory postsynaptic potentials was also reduced (44.1 +/- 13.4%, n = 14). After the PPN stimulation, these parameters immediately returned despite that the membrane hyperpolarization persisted. Iontophoretic injections of chloride ions into the motoneurons reversed the polarity of the membrane hyperpolarization during the PPN stimulation. The polarity of the outlasting hyperpolarization however was not reversed. These findings suggest that a postsynaptic inhibitory mechanism, which was mediated by chloride ions, was acting on hindlimb motoneurons during PPN-induced postural atonia. However the outlasting motoneuron hyperpolarization was not due to the postsynaptic inhibition but it could be due to a decrease in the activity of descending excitatory systems. The functional role of the PPN in the regulation of postural muscle tone is discussed with respect to the control of behavioral states of animals.

摘要

我们之前曾报道,对脚桥被盖核(PPN)腹侧部分进行电刺激会在急性去大脑猫中产生姿势性肌张力缺失[《神经科学》119(2003)293]。本研究旨在阐明PPN刺激诱发姿势性肌张力缺失期间作用于运动神经元的突触机制。对支配伸肌和屈肌的72个后肢运动神经元进行细胞内记录,并检测PPN刺激后运动神经元兴奋性的变化。对PPN进行重复电刺激(20 - 50微安,50赫兹,5 - 10秒)使伸肌和屈肌运动神经元的膜电位超极化2.0 - 12毫伏(6.0±2.3毫伏,n = 72)。即使刺激终止后,膜超极化仍持续10 - 20秒。在PPN刺激期间,膜超极化与运动神经元的放电能力(n = 28)和输入电阻(28.5±6.7%,n = 14)降低有关。此外,Ia兴奋性突触后电位的幅度也降低了(44.1±13.4%,n = 14)。PPN刺激后,尽管膜超极化持续存在,但这些参数立即恢复。向运动神经元离子导入氯离子可逆转PPN刺激期间膜超极化的极性。然而,持久超极化的极性并未逆转。这些发现表明,一种由氯离子介导的突触后抑制机制在PPN诱发的姿势性肌张力缺失期间作用于后肢运动神经元。然而,运动神经元的持久超极化并非由于突触后抑制,而是可能由于下行兴奋性系统的活动降低。关于动物行为状态的控制,讨论了PPN在姿势性肌肉张力调节中的功能作用。

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