Biomedical Engineering Department, University of Southern California, Los Angeles, CA 90089.
Biokinesiology and Physical Therapy Department, University of Southern California, Los Angeles, CA 90033.
Proc Natl Acad Sci U S A. 2024 Aug 20;121(34):e2321659121. doi: 10.1073/pnas.2321659121. Epub 2024 Aug 8.
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 multiarticular 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) coactivation or (ii) an alternative α-MN collateral projection to homonymous γ-MNs. We conclude that such α-MN collaterals are a physiologically tenable propriospinal circuit in the mammalian fusimotor system. These collaterals could still collaborate with α-γ coactivation, 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.
初级运动皮层在自主运动期间不会单独或直接产生对肌肉的α运动神经元（α-MN）驱动。相反，α-MN 驱动源自来自多个下行束、脊髓中间神经元、感觉输入和本体感受传入的兴奋性和抑制性输入的合成和竞争。一种这样的基本输入是伸展反射，即在伸展肌肉中，伸展反射应该被抑制以实现自主运动。然而，一个悬而未决的问题是，未调制的伸展反射在多大程度上破坏自主运动，以及它们在具有多个多关节肌肉的肢体中是否以及如何被抑制。我们使用恒河猴手臂的计算模型来模拟仅具有前馈α-MN 命令的运动，以及添加了速度相关的伸展反射反馈。我们发现，速度相关的伸展反射会导致手臂运动产生特定的、通常较大且可变的运动障碍。当调节速度相关的伸展反射反馈时（i）按照通常提出的（但尚未阐明）理想化的α-γ（α-γ）共激活或（ii）替代的α-MN 侧支投射到同源γ-MN 时，这些干扰会大大减少。我们得出的结论是，这种α-MN 侧支是哺乳动物牵张反射系统中具有生理可行性的固有脊髓回路。这些侧支仍然可以与α-γ 共激活以及哺乳动物中的少数骨骼牵张神经元（β-MN）协作，创建一个灵活的牵张反射生态系统以实现自主运动。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，这些侧支可以通过脑干、小脑和皮质机制成为学习、适应和表现的关键低级推动者。
