Abstract:
The primary motor cortex does not uniquely or directly produce alpha motoneurone (α-MN) drive to muscles during voluntary movement. Rather, α-MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening muscles, which should be inhibited to enable voluntary movement. It remains an open question, however, the extent to which unmodulated stretch reflexes disrupt voluntary movement, and whether and how they are inhibited in limbs with numerous multi-articular muscles. We used a computational model of a Rhesus Macaque arm to simulate movements with feedforward α-MN commands only, and with added velocity-dependent stretch reflex feedback. We found that velocity-dependent stretch reflex caused movement-specific, typically large and variable disruptions to arm movements. These disruptions were greatly reduced when modulating velocity-dependent stretch reflex feedback (i) as per the commonly proposed (but yet to be clarified) idealized alpha-gamma (α-γ) co-activation or (ii) an alternative α-MN collateral projection to homonymous γ-MNs. We conclude that such α-MN collaterals are a physiologically tenable, but previously unrecognized, propriospinal circuit in the mammalian fusimotor system. These collaterals could still collaborate with α-γ co-activation, and the few skeletofusimotor fibers (β-MNs) in mammals, to create a flexible fusimotor ecosystem to enable voluntary movement. By locally and automatically regulating the highly nonlinear neuro-musculo-skeletal mechanics of the limb, these collaterals could be a critical low-level enabler of learning, adaptation, and performance via higher-level brainstem, cerebellar and cortical mechanisms.
摘要:
在自主运动过程中,初级运动皮层不会唯一或直接产生对肌肉的α-MN驱动。相反,α-MN驱动来自多个下降道的兴奋性和抑制性输入之间的合成和竞争,脊髓中间神经元,感官输入,和本体感受传入。一个这样的基本输入是延长(拮抗)肌肉的速度依赖性拉伸反射,缩短(激动剂)肌肉被认为会抑制以允许自主运动。这仍然是一个悬而未决的问题,然而,依赖于速度的伸展反射在多大程度上扰乱了自主运动,以及是否以及如何在具有许多单关节和多关节肌肉的肢体中抑制它们,其中激动剂和拮抗剂的作用变得不清楚,并且可以在运动过程中切换。我们在恒河猴手臂的肌肉计算模型中使用3D运动对抗重力来解决这些长期存在的基本问题。在使用前馈α-MN命令模拟手臂工作区1100次不同的运动后,我们计算了由添加正的同义肌肉速度反馈引起的手臂端点轨迹的运动学中断(即,简单的速度相关拉伸反射)在不同的静态增益下对前馈α-MN驱动(没有相互抑制)。我们发现手臂终点轨迹在令人惊讶的特定运动中被破坏,通常是大的和可变的方式,甚至可以随着反射增益的增加而改变运动方向。相比之下,当通过α-MN驱动到每个肌肉(相当于其同源γ-MN的α-MN兴奋性侧支,但与α-γ共激活不同)。我们认为这个电路在神经解剖学上更站得住脚,可推广,并且比α-γ共激活和运动特异性相互抑制可扩展。事实上,我们认为,同义本脊水平的这一机制可能是通过小脑和皮质机制进行学习的关键的低级推动者,通过局部和自动调节肢体的高度非线性神经-肌肉-骨骼力学.这种固有脊髓机制还提供了一个强大的范例,可以开始阐明γ-MN驱动的失调如何导致神经系统疾病中自愿运动的中断。
■肌肉传入问题长期以来一直是一个未解决的问题,和自愿运动控制的基础。例如,未调节的速度依赖性拉伸反射如何破坏自主运动,以及如何在具有众多单关节和多关节肌肉的肢体中抑制它们,在这些肌肉中,激动剂和拮抗剂的作用变得不清楚,并且可以在运动过程中切换仍不清楚.在这里,我们展示了不受调节的速度相关反射的成本,并提出了一种低水平的本体脊髓机制,可以规范这些错误并实现运动学习和表现。我们的结果表明,通过同源α-MN侧支缩放动态γ-MN的这种脊髓水平机制提供了一种可推广的机制,可能是准确和可预测的运动的低水平推动者,可以局部稳定并补充合成和竞争皮层之间的竞争,对α-MN池的皮质下或本体脊髓投射。