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首页> 外文期刊>Brain research. Brain research reviews >Spinal interneurones; how can studies in animals contribute to the understanding of spinal interneuronal systems in man?
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Spinal interneurones; how can studies in animals contribute to the understanding of spinal interneuronal systems in man?

机译:脊髓中神经元;在动物中进行的研究如何有助于理解人的脊髓神经内系统?

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The first part of this review deals with arguments that the essential properties and organization of spinal interneuronal systems in the cat and in man are similar. The second part is concerned with the possibility that some interneuronal systems may be responsible for motor disturbances caused by spinal cord injuries and that these interneurones may be defined. This possibility is discussed with respect to the hyperexcitability of alpha-motoneurones and the exaggeration of stretch reflexes in spastic patients. To this end, what is known about cat spinal interneurones and about the neuronal basis and pharmacological treatment of spasticity, is put together. Interneurones in di- and trisynaptic reflex pathways from group II muscle afferents are singled out, since they are depressed by the alpha(2) noradrenaline receptor agonists clonidine and tizanidine, which is a critical feature of interneurones expected to contribute to exaggerated stretch reflexes which are reduced by alpha(2) noradrenaline receptor agonists. Recent observations that reflex excitation of extensor motoneurones from group II afferents is enhanced in spastic patients and that the pathologically strong reflex actions of group II afferents are reduced by clonidine and tizanidine support this proposal. On the other hand, a lack of effect of clonidine and tizanidine upon other types of excitatory or inhibitory interneurones argues against any major contribution of such interneurones to the abnormally strong responses of alpha-motoneurones to muscle stretch.
机译:这篇综述的第一部分讨论的论点是,猫和人中脊髓神经元间系统的基本特性和组织都相似。第二部分涉及某些神经内系统可能对由脊髓损伤引起的运动障碍负责,并可能定义了这些神经元的可能性。关于α-运动神经元的过度兴奋性和痉挛性患者中过度伸展反应的讨论,讨论了这种可能性。为此,将有关猫脊髓中枢神经节以及神经元基础和痉挛的药理学治疗的知识汇总在一起。组II肌肉传入神经突触和三突触反射通路中的中间神经元被挑出,因为它们被α(2)去甲肾上腺素受体激动剂可乐定和替扎尼定抑制,这是中间神经元的关键特征,预计会导致过度的拉伸反射。被alpha(2)去甲肾上腺素受体激动剂减少。最近的观察结果表明,痉挛患者增强了II组传入神经的伸肌运动神经元的反射兴奋,可乐定和替扎尼定降低了II组传入神经的病理性强反射作用,支持了这一提议。另一方面,可乐定和替扎尼定对其他类型的兴奋性或抑制性中枢神经元缺乏作用,反对此类中枢神经元对α-运动神经元对肌肉拉伸的异常强烈反应的任何主要贡献。

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