The functionality and cerebral capacity of the central nervous system (CNS) depend on complex interactions of astrocytes with neurons and other cell types¹. While their intercellular communication is well described with respect to certain signalling molecules, very little is known about how astrocytes use intracellular membrane trafficking pathways to orchestrate and exert multiple functions. We discovered an elaborate membrane compartment of tubular endosomes in astrocytes. These membrane tubules are associated with Rab8 GTPases, which are involved in various diseases, including Parkinson’s disease. Tubular Rab8+ membrane compartments act as trafficking hubs for surface receptors and adhesion molecules, including β1-integrin². Rab8+ membrane tubule formation involves the leucine-rich repeat kinase 2 (LRRK2) and requires the reorganisation of membrane-associated cytoskeletal scaffolds via the actin regulator drebrin. Perturbances in Drebrin-Rab8-dependent membrane trafficking cause profound defects in vivo: Following CNS injuries, drebrin loss leads to atherosclerosis-like membrane accumulations in astrocytes, followed by the disruption of astrocyte reactivity and the development of excessive neurodegeneration^2,3. Moreover, drebrin loss impairs the organisation of cerebral blood vessels and blood-brain barrier integrity. In summary, our work shows that cytoskeleton-assisted membrane trafficking in astrocytes is an important mechanism in sustaining neuronal networks and the neurovasculature.