Objective : Müller glial cells in the retinas of teleost fish and amphibians possess stem cell-like properties that enable regeneration following injury or degeneration. In mammals, however, this regenerative capacity is severely limited. In a recent study, we demonstrated that microglia-derived inflammatory cytokines are essential for triggering Müller cell quiescence exit in the degenerating mouse retina. We now aim at investigating the mechanisms underlying this inflammation/regeneration coupling, with a focus on Notch signaling. This pathway is already known to act cell-autonomously in Müller glial cells. However, we put forward a novel hypothesis, namely that Notch pathway might also indirectly affect Müller glia response to injury by regulating neuroinflammatory signaling in microglial cells. Methods : As a model of degeneration, we used retinal explants from mice expressing a fluorescent reporter gene in microglia and analysed phenotypes by RNAseq, RT-qPCR and immunofluorescence. Results : We found that components of the Notch signaling pathway are indeed expressed in retinal microglia. Preliminary functional analyses indicate that Notch signaling in these microglial cells regulates their proliferation and activation states and modulates their cytokine expression profile. Conclusion : These findings suggest that, beyond its well-established cell-autonomous role in Müller cells, Notch signalling within microglia plays a pivotal role in shaping the retinal microenvironment and may as such indirectly influence the regenerative potential of Müller glia.