In vivo imaging of the rodent spinal cord has advanced our understanding of how resident cells of the central nervous system (CNS) respond to neuroinflammation. By combining two-photon imaging and experimental autoimmune encephalomyelitis (EAE), the most widely used rodent model of multiple sclerosis (MS), it has been possible, for example, to study how axons degenerate when confronted with inflammatory cells, how oligodendrocytes get damaged in inflammatory lesions, and how immune cells themselves adapt their phenotype and functionality to the changing lesion environment. Similar approaches are now increasingly used to study other forms of neuroinflammation, such as antibody/complement-mediated neuromyelitis optica spectrum disease (NMOSD). To tackle the most pressing open questions in the field, new biosensors and indicator mice that report the metabolic state and interaction of cells in neuroinflammatory lesions are being developed. Moreover, the field is moving towards new anatomical sites of inflammation, such as the cortical gray matter, but also towards longer observation intervals to reveal the chronic perturbations and adaptations that characterize advanced stages of MS.      «

In vivo imaging of the rodent spinal cord has advanced our understanding of how resident cells of the central nervous system (CNS) respond to neuroinflammation. By combining two-photon imaging and experimental autoimmune encephalomyelitis (EAE), the most widely used rodent model of multiple sclerosis (MS), it has been possible, for example, to study how axons degenerate when confronted with inflammatory cells, how oligodendrocytes get damaged in inflammatory lesions, and how immune cells themsel...     »