Rybak Ilya A, Shevtsova Natalia A, Lafreniere-Roula Myriam, McCrea David A
Department of Neurobiology and Anatomy, Drexel University College of Medicine, Philadelphia, PA 19129, USA.
J Physiol. 2006 Dec 1;577(Pt 2):617-39. doi: 10.1113/jphysiol.2006.118703. Epub 2006 Sep 28.
The mammalian spinal cord contains a locomotor central pattern generator (CPG) that can produce alternating rhythmic activity of flexor and extensor motoneurones in the absence of rhythmic input and proprioceptive feedback. During such fictive locomotor activity in decerebrate cats, spontaneous omissions of activity occur simultaneously in multiple agonist motoneurone pools for a number of cycles. During these 'deletions', antagonist motoneurone pools usually become tonically active but may also continue to be rhythmic. The rhythmic activity that re-emerges following a deletion is often not phase shifted. This suggests that some neuronal mechanism can maintain the locomotor period when motoneurone activity fails. To account for these observations, a simplified computational model of the spinal circuitry has been developed in which the locomotor CPG consists of two levels: a half-centre rhythm generator (RG) and a pattern formation (PF) network, with reciprocal inhibitory interactions between antagonist neural populations at each level. The model represents a network of interacting neural populations with single interneurones and motoneurones described in the Hodgkin-Huxley style. The model reproduces the range of locomotor periods and phase durations observed during real locomotion in adult cats and permits independent control of the level of motoneurone activity and of step cycle timing. By altering the excitability of neural populations within the PF network, the model can reproduce deletions in which motoneurone activity fails but the phase of locomotor oscillations is maintained. The model also suggests criteria for the functional identification of spinal interneurones involved in the mammalian locomotor pattern generation.
哺乳动物的脊髓包含一个运动中枢模式发生器（CPG），在没有节律性输入和本体感受反馈的情况下，它能够产生屈肌和伸肌运动神经元的交替节律性活动。在去大脑猫的这种虚构运动活动期间，多个主动肌运动神经元池会在多个周期内同时出现自发的活动缺失。在这些“缺失”期间，拮抗肌运动神经元池通常会变得紧张性活跃，但也可能继续保持节律性。缺失后重新出现的节律性活动通常不会发生相位偏移。这表明当运动神经元活动失败时，某些神经元机制可以维持运动周期。为了解释这些观察结果，已经开发了一种简化的脊髓回路计算模型，其中运动CPG由两个层次组成：一个半中枢节律发生器（RG）和一个模式形成（PF）网络，在每个层次上，拮抗神经群体之间存在相互抑制性相互作用。该模型代表了一个相互作用的神经群体网络，其中单个中间神经元和运动神经元采用霍奇金-赫胥黎风格进行描述。该模型再现了成年猫实际运动期间观察到的运动周期范围和相位持续时间，并允许独立控制运动神经元活动水平和步周期时间。通过改变PF网络内神经群体的兴奋性，该模型可以再现运动神经元活动失败但运动振荡相位得以维持的缺失情况。该模型还提出了用于功能性识别参与哺乳动物运动模式生成的脊髓中间神经元的标准。
