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首页> 外文期刊>Neuroscience: An International Journal under the Editorial Direction of IBRO >Changes in the excitability of hindlimb motoneurons during muscular atonia induced by stimulating the pedunculopontine tegmental nucleus in cats.
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Changes in the excitability of hindlimb motoneurons during muscular atonia induced by stimulating the pedunculopontine tegmental nucleus in cats.

机译:刺激猫的足弓形被盖核诱导的肌肉无力时后肢运动神经元的兴奋性变化。

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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.
机译:我们先前曾报道过,电刺激传递到足小脑桥骨被膜核(PPN)的腹侧部分会在急性去脑猫中产生体位性心律失常[Neuroscience 119(2003)293]。本研究旨在阐明在PPN刺激引起的姿势性心律失常期间作用于运动神经元的突触机制。从72个支配伸肌和屈肌的后肢运动神经元进行细胞内记录,并检查PPN刺激后运动神经元的兴奋性变化。 PPN的重复电刺激(20-50 microA,50 Hz,5-10 s)使伸肌和屈肌神经元的膜电位超极化2.0-12 mV(6.0 +/- 2.3 mV,n = 72)。甚至在刺激终止后,膜超极化仍持续10-20 s。在PPN刺激期间,膜超极化与运动神经元的射击能力(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)。在PPN刺激后,尽管膜超极化持续存在,但这些参数立即返回。在PPN刺激过程中,向运动神经元中离子注入氯离子可逆转膜超极化的极性。然而,持久的超极化的极性没有反转。这些发现表明,由氯离子介导的突触后抑制机制在PPN诱导的姿势性心律失常期间作用于后肢运动神经元。然而,持久的运动神经元超极化不是由于突触后抑制,而是由于下降的兴奋性系统活性降低。关于控制动物的行为状态,讨论了PPN在姿势性肌张力调节中的功能作用。

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