Wright Patrick W, Archambault Angela S, Peek Stacey, Bauer Adam Q, Culican Susan M, Ances Beau M, Culver Joseph P, Wu Gregory F
Department of Radiology, Washington University in St. Louis School of Medicine, United States.
Department of Neurology, Washington University in St. Louis School of Medicine, United States.
Exp Neurol. 2017 Sep;295:18-22. doi: 10.1016/j.expneurol.2017.05.004. Epub 2017 May 11.
The basis for neuronal dysfunction following inflammatory demyelination of the central nervous system (CNS) remains poorly understood. We characterized the network response to white matter injury in the anterior visual pathway using an experimental model of optic neuritis (ON), as ON is often an early manifestation of immune-mediated CNS demyelination in multiple sclerosis (MS). Optical intrinsic signal imaging was performed before and after the induction of ON in mice to measure changes in cortical network functional connectivity. We observed a greater loss of connectivity between homotopic visual cortices in ON mice compared to controls. Further, decreases in homotopic visual cortex connectivity were associated with visual acuity loss in ON mice. These results demonstrate that network connectivity changes resulting from ON can be modeled in an experimental murine system. Future studies will identify the mechanisms that cause neuronal dysfunction due to white matter injury seen in MS.
中枢神经系统（CNS）炎性脱髓鞘后神经元功能障碍的基础仍知之甚少。我们使用视神经炎（ON）的实验模型，对前视觉通路中白质损伤的网络反应进行了表征，因为ON通常是多发性硬化症（MS）中免疫介导的CNS脱髓鞘的早期表现。在小鼠诱导ON之前和之后进行光学内在信号成像，以测量皮质网络功能连接性的变化。与对照组相比，我们观察到ON小鼠同侧视觉皮层之间的连接性损失更大。此外，同侧视觉皮层连接性的降低与ON小鼠的视力丧失有关。这些结果表明，ON导致的网络连接性变化可以在实验性小鼠系统中进行模拟。未来的研究将确定导致MS中所见白质损伤引起神经元功能障碍的机制。
