Department of Neuroscience, Cell Biology and Physiology, Wright State University, Dayton, Ohio.
Ann N Y Acad Sci. 2018 Jan;1412(1):170-177. doi: 10.1111/nyas.13472. Epub 2017 Oct 5.
A number of studies in the past 20 years have shown that perturbation of activity of the nervous system leads to compensatory changes in synaptic strength that serve to return network activity to its original level. This response has been termed homeostatic synaptic plasticity. Despite the intense interest in homeostatic synaptic plasticity, little attention has been paid to its role in the prototypic synaptic disease, myasthenia gravis. In this review, we discuss mechanisms that have been shown to mediate homeostatic synaptic plasticity at the mammalian neuromuscular junction. A subset of these mechanisms have been shown to occur in myasthenia gravis. The homeostatic changes occurring in myasthenia gravis appear to involve the presynaptic nerve terminal and may even involve changes in the excitability of motor neurons within the spinal cord. The finding of presynaptic homeostatic synaptic plasticity in myasthenia gravis leads us to propose that changes in the motor unit in myasthenia gravis may be more widespread than previously appreciated.
过去 20 年来的多项研究表明，神经系统活动的扰乱会导致突触强度的代偿性变化，从而使网络活动恢复到原来的水平。这种反应被称为同型突触可塑性。尽管人们对同型突触可塑性非常感兴趣，但很少关注其在典型突触疾病——重症肌无力中的作用。在这篇综述中，我们讨论了已被证明可在哺乳动物神经肌肉接点处介导同型突触可塑性的机制。其中一些机制已被证明在重症肌无力中发生。重症肌无力中发生的同型变化似乎涉及突触前神经末梢，甚至可能涉及脊髓内运动神经元兴奋性的变化。在重症肌无力中发现的突触前同型突触可塑性使我们提出，重症肌无力中运动单位的变化可能比以前认为的更为广泛。
