Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Neurobiol Dis. 2010 Sep;39(3):252-64. doi: 10.1016/j.nbd.2010.03.021. Epub 2010 Apr 8.
In amyotrophic lateral sclerosis (ALS), the exogenous temporal triggers that result in initial motor neuron death are not understood. Overactivation and consequent accelerated loss of vulnerable motor neurons is one theory of disease initiation. The vulnerability of motor neurons in response to chronic peripheral nerve hyperstimulation was tested in the SOD1(G93A) rat model of ALS. A novel in vivo technique for peripheral phrenic nerve stimulation was developed via intra-diaphragm muscle electrode implantation at the phrenic motor endpoint. Chronic bilateral phrenic nerve hyperstimulation in SOD1(G93A) rats accelerated disease progression, including shortened lifespan, hastened motor neuron loss and increased denervation at diaphragm neuromuscular junctions. Hyperstimulation also resulted in focal decline in adjacent forelimb function. These results show that peripheral phrenic nerve hyperstimulation accelerates cell death of vulnerable spinal motor neurons, modifies both temporal and anatomical onset of disease, and leads to involvement of disease in adjacent anatomical regions in this ALS model.
在肌萎缩侧索硬化症(ALS)中,导致初始运动神经元死亡的外源性时间触发因素尚不清楚。过度激活和随之而来的易损运动神经元加速丧失是疾病起始的一种理论。通过在膈神经运动终末处进行膈肌内电极植入,开发了一种新的体内膈神经刺激技术,用于测试 ALS 的 SOD1(G93A) 大鼠模型中易损运动神经元对慢性周围神经过度刺激的反应。慢性双侧膈神经过度刺激加速了 SOD1(G93A) 大鼠的疾病进展,包括缩短寿命、加速运动神经元丧失和膈神经肌肉接头去神经支配增加。过度刺激还导致相邻前肢功能出现局部下降。这些结果表明,周围膈神经过度刺激加速了易损脊髓运动神经元的细胞死亡,改变了疾病的时间和解剖学发病,导致疾病在该 ALS 模型中涉及相邻解剖区域。