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

虽然神经元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，神经胶质细胞的功能是由一个复杂的时间和空间安排的钙信号。Ca 2+调节异常是神经炎性疾病（包括多发性硬化症（MS））的常见现象。实验性自身免疫性脑脊髓炎（EAE）和毒性铜腙诱发的脱髓鞘是模拟人类疾病的不同组分（例如炎症或髓鞘再生）的两种动物模型。使用在体内双光子激光扫描显微镜（2 P-LSM）和基因修饰的小鼠与细胞特异性遗传编码的Ca 2+指示剂表达，我们将分析自发和诱发的Ca 2+信号的少突胶质细胞，星形胶质细胞和小胶质细胞在两个MS模型的脊髓束内。识别潜在的分子途径在体内将有助于理解MS的复杂的病理机制，并将提供新的选择，为发展的治疗策略。

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.