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Streitberg, Axel von (2016): The response of NG2-glia after traumatic brain injury. Dissertation, LMU München: Faculty of Biology



The mammalian central nervous system (CNS) consists of many different cell types contributing to its complex functional outcome. Its task of controlling essential body functions led to a unique cellular composition of this organ with many tissue-specific properties. One of the resulting consequences is an altered response to tissue damage, leading to insufficient regeneration following CNS injuries or diseases, which yields detrimental outcome for the majority of brain pathologies. A CNS-specific cell type which has just recently been connected to injury response are the NG2-glia. So far, these cells were known to be the major proliferative pool outside the neurogenic niches and are furthermore the progenitors of oligodendrocytes in the adult brain parenchyma. Given their great abundance, it is of major importance to better characterize the behavior and functionality of NG2-glia especially in relation to brain injury. Therefore, the aim of this PhD thesis was to further the knowledge about the course of events and potential functions of the NG2-glia response following traumatic brain injury. A detailed analysis of the cellular events employing in vivo two-photon microscopy in stab wounded mice expressing GFP within the oligodendrocyte lineage, revealed a fast and heterogeneous response of the majority of NG2-glia. The cells showed different behaviors like hypertrophy, polarization, migration and proliferation; whereas a small subset of NG2-glia and all mature oligodendrocytes remained static, retaining their initial position and morphology. The intensity of the observed injury response of NG2-glia was dependent on the severity of tissue damage as well as the distance to the injury. During the peak of NG2-glia reactivity that was observed between 2-4 days after injury an accumulation of NG2-glia directly within and in very close proximity to the lesion core could be detected. This cellular amassment led to a transient discontinuity of the homeostatic control of NG2-glia, which had been observed under physiological conditions. While starting from one week after injury, this cellular homeostasis was progressively reinstated and completely restored one month later. These events of cellular accumulation of NG2-glia after brain injury argue for the contribution to a first scaffold that is built after tissue damage, probably participating in wound closure and highlighting their importance in brain pathology.