Astrocytes are generally accepted as important players in synaptic function and development. On the other hand astrocytes in vivo have a very complex 3D structure, which is shaped by their numerous and highly ramified thin peripheral processes. Morphology of perisynaptic astrocytic processes (PAP) is subject to constant remodeling, for instance, long-lasting PAP retraction in hypothalamus is known to alter synaptic transmission and deficiency in PAP movement can prevent dendritic spine formation and synaptic maturation. The PAP motility is likely to be actin-based since they are known to contain actin and actin-related proteins. We use actinbinding deficient Profilin-1 (abdProf-1) as a genetically-encodable tool to selectively suppress activity-dependent morphological plasticity of astrocytes in combination with membrane targeted form of GFP (LckGFP) to trace PAPs precisely. This approach combined with astrocyte-specific viral gene delivery allows us to learn how suppressed morphological response of astrocytes can affect synaptic function in the mouse brain.