Takakusaki K, Kohyama J, Matsuyama K, Mori S
Department of Physiology, Asahikawa Medical College, 078-8510, Asahikawa, Japan.
Neuroscience. 2001;103(2):511-27. doi: 10.1016/s0306-4522(00)00586-8.
The present study was designed to elucidate the spinal interneuronal mechanisms of motor inhibition evoked by stimulating the medullary reticular formation. Two questions were addressed. First, whether there is a parallel motor inhibition to motoneurons and to interneurons in reflex pathways. Second, whether the inhibition is mediated by interneurons interposed in known reflex pathways. We recorded the intracellular activity of hindlimb motoneurons in decerebrate cats and examined the effects of medullary stimulation on these neurons and on interneuronal transmission in reflex pathways to them. Stimuli (three pulses at 10-60microA and 1-10ms intervals) delivered to the nucleus reticularis gigantocellularis evoked inhibitory postsynaptic potentials in alpha-motoneurons (n=147) and gamma-motoneurons (n=5) with both early and late latencies. The early inhibitory postsynaptic potentials were observed in 66.4% of the motoneurons and had a latency of 4.0-5.5ms with a segmental delay of more than 1.4ms. The late inhibitory postsynaptic potentials were observed in 98.0% of the motoneurons and had a latency of 30-35ms, with a peak latency of 50-60ms. Both types of inhibitory postsynaptic potentials were evoked through fibers descending in the ventrolateral quadrant. The inhibitory postsynaptic potentials were not influenced by recurrent inhibitory pathways, but both types were greatly attenuated by volleys in flexor reflex afferents. Conditioning medullary stimulation, which was subthreshold to evoke inhibitory postsynaptic potentials in the motoneurons, neither evoked primary afferent depolarization of dorsal roots nor reduced the input resistance of the motoneurons. However, the conditioning stimulation often facilitated non-reciprocal group I inhibitory pathways (Ib inhibitory pathways) to the motoneurons in early (<20ms) and late (30-80ms) periods. In contrast, it attenuated test postsynaptic potentials evoked through reciprocal Ia inhibitory pathways, and excitatory and inhibitory pathways from flexor reflex afferent and recurrent inhibitory pathways. The inhibitory effects were observed in both early and late periods. The present results provide new information about a parallel inhibitory process from the medullary reticular formation that produces a generalized motor inhibition by acting on alpha- and gamma-motoneurons, and on interneurons in reflex pathways. Interneurons receiving inhibition from flexor reflex afferents and a group of Ib interneurons may mediate the inhibitory effects upon motoneurons.
本研究旨在阐明刺激延髓网状结构所诱发的运动抑制的脊髓中间神经元机制。研究探讨了两个问题。第一，在反射通路中，对运动神经元和中间神经元的运动抑制是否并行。第二，这种抑制是否由已知反射通路中的中间神经元介导。我们记录了去大脑猫后肢运动神经元的细胞内活动，并研究了延髓刺激对这些神经元以及对通向它们的反射通路中中间神经元传递的影响。施加于巨细胞网状核的刺激（10 - 60微安、间隔1 - 10毫秒的三个脉冲）在α运动神经元（n = 147）和γ运动神经元（n = 5）中诱发了抑制性突触后电位，潜伏期有早有晚。66.4%的运动神经元出现了早期抑制性突触后电位，潜伏期为4.0 - 5.5毫秒，节段延迟超过1.4毫秒。98.0%的运动神经元出现了晚期抑制性突触后电位，潜伏期为30 - 35毫秒，峰值潜伏期为50 - 60毫秒。两种类型的抑制性突触后电位都是通过腹外侧象限下行的纤维诱发的。抑制性突触后电位不受返回抑制通路的影响，但两种类型都因屈肌反射传入冲动的发放而大大减弱。对运动神经元诱发抑制性突触后电位阈下的条件性延髓刺激，既不诱发背根的初级传入去极化，也不降低运动神经元的输入电阻。然而，条件性刺激在早期（<20毫秒）和晚期（30 - 80毫秒）常常易化通向运动神经元的非交互性I组抑制通路（Ib抑制通路）。相反，它减弱了通过交互性Ia抑制通路、屈肌反射传入的兴奋和抑制通路以及返回抑制通路诱发的测试突触后电位。在早期和晚期都观察到了抑制作用。目前的结果提供了关于来自延髓网状结构的并行抑制过程的新信息，该过程通过作用于α和γ运动神经元以及反射通路中的中间神经元产生广泛的运动抑制。接受屈肌反射传入抑制的中间神经元和一组Ib中间神经元可能介导了对运动神经元的抑制作用。
