Astrocytes have a distinct complex, branched morphology. Pathological injury in the central nervous system induces a process called astrogliosis in astrocytes, in which their morphology becomes less complex, with larger cell bodies and fewer fine processes; the mechanism behind these morphological changes is unknown. On page 3873, Jonathan Hanley and colleagues ask how the actin machinery that typically promotes the outwards movement of the plasma membrane in astrocytes is involved in maintaining astrocyte complexity and in the morphological changes that occur during astrogliosis. The authors focus on the actin-nucleating complex Arp2/3, and show that its inhibition leads to rapid expansion of astrocyte cell bodies and major processes in culture and brain tissue. This expansion required functional myosin II downstream of the small GTPase RhoA and Rho-dependent kinase (ROCK). In a series of knockdown experiments to investigate which endogenous Arp2/3 regulatory proteins are required to maintain astrocyte morphology, the authors find that cell body expansion and reduced morphological complexity are induced in the absence of the Arp2/3 subunit Arp3 or the Arp2/3 activator N-WASP. Depletion of WAVE2 specifically reduced astrocyte branching complexity but, conversely, knockdown of the Arp2/3 inhibitor PICK1 increased the branching complexity. Moreover, ischaemia-induced astrocyte expansion was delayed by knockdown of PICK1 or overexpression of N-WASP. These findings show that astrocytes use a balance of Arp2/3 activation and inhibition through N-WASP, WAVE2 and PICK1 to control the complexity of their morphology, and this mechanism underlies the morphological changes to astrocytes induced by pathological insult.