Department of Cell Biology, Whitehead Biomedical Research Building, Emory University School of Medicine, Atlanta, GA, USA.
Adv Neurobiol. 2022;28:87-107. doi: 10.1007/978-3-031-07167-6_4.
Homeostatic plasticity represents a set of compensatory mechanisms that are engaged following a perturbation to some feature of neuronal or network function. Homeostatic mechanisms are most robustly expressed during development, a period that is replete with various perturbations such as increased cell size and the addition/removal of synaptic connections. In this review we look at numerous studies that have advanced our understanding of homeostatic plasticity by taking advantage of the accessibility of developing motoneurons. We discuss the homeostatic regulation of embryonic movements in the living chick embryo and describe the spinal compensatory mechanisms that act to recover these movements (homeostatic intrinsic plasticity) or stabilize synaptic strength (synaptic scaling). We describe the expression and triggering mechanisms of these forms of homeostatic plasticity and thereby gain an understanding of their roles in the motor system. We then illustrate how these findings can be extended to studies of developing motoneurons in other systems including the rodents, zebrafish, and fly. Furthermore, studies in developing drosophila have been critical in identifying some of the molecular signaling cascades and expression mechanisms that underlie homeostatic intrinsic membrane excitability. This powerful model organism has also been used to study a presynaptic form of homeostatic plasticity where increases or decreases in synaptic transmission are associated with compensatory changes in probability of release at the neuromuscular junction. Further, we describe studies that demonstrate homeostatic adjustments of ion channel expression following perturbations to other kinds of ion channels. Finally, we discuss work in xenopus that shows a homeostatic regulation of neurotransmitter phenotype in developing motoneurons following activity perturbations. Together, this work illustrates the importance of developing motoneurons in elucidating the mechanisms and roles of homeostatic plasticity.
稳态可塑性代表了一组补偿机制，这些机制在神经元或网络功能的某些特征受到干扰后被激活。稳态机制在发育过程中最为强烈地表达，这个时期充满了各种干扰，如细胞大小的增加和突触连接的增加/去除。在这篇综述中，我们通过利用发育中的运动神经元的可及性，研究了许多进展，这些进展增进了我们对稳态可塑性的理解。我们讨论了活体鸡胚中胚胎运动的稳态调节，并描述了作用于恢复这些运动的脊髓补偿机制（稳态内在可塑性）或稳定突触强度（突触缩放）。我们描述了这些形式的稳态可塑性的表达和触发机制，从而了解它们在运动系统中的作用。然后，我们说明如何将这些发现扩展到其他系统（包括啮齿动物、斑马鱼和苍蝇）中发育中的运动神经元的研究中。此外，在发育中的果蝇中的研究对于确定一些分子信号级联和基础内在膜兴奋性的稳态的表达机制至关重要。这种强大的模式生物也被用于研究一种突触前形式的稳态可塑性，其中突触传递的增加或减少与神经肌肉接头处释放概率的补偿性变化相关。此外，我们描述了研究表明，在其他类型的离子通道受到干扰后，离子通道表达会发生稳态调整。最后，我们讨论了在 Xenopus 中进行的工作，该工作表明在活动干扰后，发育中的运动神经元中的神经递质表型会进行稳态调节。总之，这项工作说明了在阐明稳态可塑性的机制和作用方面，发育中的运动神经元的重要性。
