Role of glial Ca2+ signals during neuroinflammation, axonal degeneration, and de- andremyelination in the mouse spinal cord – Part II

神经网络功能在很大程度上是由不同的动作电位放电模式编码的，而神经胶质细胞的功能则是由复杂的钙信号的时间和空间排列决定的。钙调节失调是包括多发性硬化症(MS)在内的神经炎症性疾病的常见现象。实验性自身免疫性脑脊髓炎(EAE)和毒性亚铜诱发的脱髓鞘是两种模拟人类疾病不同组成部分(例如炎症或重新髓鞘形成)的动物模型。使用体内双光子激光扫描显微镜(2P-LSM)和转基因小鼠，分析两种MS模型脊髓背束内少突胶质细胞、星形胶质细胞和小胶质细胞自发和诱发的钙信号。识别体内潜在的分子通路将有助于了解MS复杂的发病机制，并将为开发治疗策略提供新的选择。

While neuronal network function is largely encoded by distinct patterns of action potential firing, glial cell functions are determined by a complex temporal and spatial arrangement of Ca2+ signals. Dysregulation of Ca2+ is a common phenomenon of neuroinflammatory diseases, including multiple sclerosis (MS). Experimental autoimmune encephalomyelitis (EAE) and toxic cuprizone-evoked demyelination are two animal models that mimic different components (e.g. inflammation or remyelination) of the human disease. Using in vivo twophoton laser-scanning microscopy (2P-LSM) and genetically modified mice with cell-specific genetically encoded Ca2+ indicator expression we will analyse spontaneous and evoked Ca2+ signals of oligodendrocytes, astrocytes and microglia within the dorsal spinal tracts in both MS models. Identification of the underlying molecular pathways in vivo will help to understand the complex pathomechanisms of MS and will provide novel options for the development of therapeutic strategies.