This study was designed to determine whether and how the sympathetic nervous system (SNS) regulates motoneuron axon function and neuromuscular transmission in young (3–4-month) and geriatric (31-month) mice. Our approach included sciatic-peroneal nerve immunolabeling coregistration, and electrophysiological recordings in a novel mouse ex-vivo preparation, the sympathetic-peroneal nerve-lumbricalis muscle (SPNL). Here, the interaction between the motoneuron and SNS at the neuromuscular junction (NMJ) and muscle innervation reflect the complexity of the living mouse. Our data show that electrical stimulation of the sympathetic neuron at the paravertebral ganglia chain enhances motoneuron synaptic vesicle release at the NMJ in young mice, while in geriatric mice, this effect is blunted. We also found that blocking β-AR prevents the sympathetic neuron from increasing NMJ transmission. Immunofluorescence coexpression analysis of immunolabeled ARs with choline acetyltransferase-, tyrosine hydroxylase-, or calcitonin gene-related peptide immunoreactive axons showed that α2B-AR is found mainly in sympathetic neurons, β1-AR in sympathetic- and motor-neurons, and both decline significantly with aging. In summary, this study unveils the molecular substrate accounting for the influence of endogenous sympathetic neurons on motoneuron-muscle transmission in young mice and its decline with aging.

中文翻译：

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β1-和α2B-肾上腺素能受体介导的老年小鼠钝性神经元突触小泡的交感神经元调节。

本研究旨在确定交感神经系统（SNS）是否以及如何调节年轻（3-4个月）和老年（31个月）小鼠的运动神经元轴突功能和神经肌肉传递。我们的方法包括坐骨神经-腓神经的免疫标记共迁移，以及新型小鼠离体制剂即交感神经-腓神经的电生理记录。（SPNL）。在这里，运动神经元和SNS在神经肌肉接头（NMJ）和肌肉神经支配之间的相互作用反映了活体小鼠的复杂性。我们的数据表明，在幼小小鼠中，对椎旁神经节链上的交感神经元的电刺激增强了运动神经元突触小泡在NMJ处的释放，而在老年小鼠中，这种作用减弱了。我们还发现，阻断β-AR可以阻止交感神经元增加NMJ传递。胆碱乙酰基转移酶，酪氨酸羟化酶或降钙素基因相关肽免疫反应性轴突对免疫标记AR的免疫荧光共表达分析表明，α2B-AR主要存在于交感神经元中，β1-AR则存在于交感神经元和运动神经元中，并且两者均显着下降随着年龄的增长。综上所述，