Clinical Laboratory for Bionic Extremity Reconstruction, Department of Plastic, Reconstructive, and Aesthetic Surgery, Medical University of Vienna, 1090 Vienna, Austria.
Centers for Biomedical Research, Medical University of Vienna, 1090 Vienna, Austria.
J Neurosci. 2022 Nov 2;42(44):8297-8307. doi: 10.1523/JNEUROSCI.0670-22.2022.
The surgical redirection of efferent neural input to a denervated muscle via a nerve transfer can reestablish neuromuscular control after nerve injuries. The role of autonomic nerve fibers during the process of muscular reinnervation remains largely unknown. Here, we investigated the neurobiological mechanisms behind the spontaneous functional recovery of denervated facial muscles in male rodents. Recovered facial muscles demonstrated an abundance of cholinergic axonal endings establishing functional neuromuscular junctions. The parasympathetic source of the neuronal input was confirmed to be in the pterygopalatine ganglion. Furthermore, the autonomically reinnervated facial muscles underwent a muscle fiber change to a purely intermediate muscle fiber population myosin heavy chain type IIa. Finally, electrophysiological tests revealed that the postganglionic parasympathetic fibers travel to the facial muscles via the sensory infraorbital nerve. Our findings demonstrated expanded neuromuscular plasticity of denervated striated muscles enabling functional recovery via alien autonomic fibers. These findings may further explain the underlying mechanisms of sensory protection implemented to prevent atrophy of a denervated muscle. Nerve injuries represent significant morbidity and disability for patients. Rewiring motor nerve fibers to other target muscles has shown to be a successful approach in the restoration of motor function. This demonstrates the remarkable capacity of the CNS to adapt to the needs of the neuromuscular system. Yet, the capability of skeletal muscles being reinnervated by nonmotor axons remains largely unknown. Here, we show that under deprivation of original efferent input, the neuromuscular system can undergo functional and morphologic remodeling via autonomic nerve fibers. This may explain neurobiological mechanisms of the sensory protection phenomenon, which is because of parasympathetic reinnervation.
通过神经转移将传出神经输入重新导向去神经肌肉，可以在神经损伤后重新建立神经肌肉控制。自主神经纤维在肌肉再支配过程中的作用在很大程度上尚不清楚。在这里，我们研究了雄性啮齿动物去神经面部肌肉自发功能恢复背后的神经生物学机制。恢复的面部肌肉表现出丰富的胆碱能轴突末端，建立功能性神经肌肉接头。神经元输入的副交感神经来源被确认为翼腭神经节。此外，自主再支配的面部肌肉经历了肌纤维向纯中间肌纤维群肌球蛋白重链 IIa 的变化。最后，电生理测试显示节后副交感纤维通过感觉眶下神经到达面部肌肉。我们的研究结果表明，去神经横纹肌具有扩展的神经肌肉可塑性，能够通过外来自主纤维实现功能恢复。这些发现可能进一步解释了实施感觉保护以防止去神经肌肉萎缩的潜在机制。神经损伤对患者的发病率和残疾有重大影响。将运动神经纤维重新连接到其他靶肌肉已被证明是恢复运动功能的成功方法。这表明中枢神经系统有能力适应神经肌肉系统的需求。然而，骨骼肌被非运动轴突再支配的能力在很大程度上尚不清楚。在这里，我们表明在剥夺原始传出输入的情况下，神经肌肉系统可以通过自主神经纤维进行功能和形态重塑。这可以解释感觉保护现象的神经生物学机制，因为这是由于副交感神经再支配。
