Purinergic receptors are widely expressed in the central nervous system, where they stimulate processes such as inflammation and neurotransmission. Little is known, however, about their involvement in mediating axon elongation during development and following injury. On page 176, Juan José Garrido and co-workers now shed light on the mechanisms that coordinate axon elongation downstream of purinergic receptors. They reported previously, that inhibition of the ionotropic, ATP-operated P2X7 receptor promotes axon growth. Using a combination of pharmacological and molecular biological approaches, they now show that the activation of the metabotropic P2Y13 receptor by ADP also has a negative effect on axonal elongation, whereas the metabotropic P2Y1 receptor has the opposing effect and stimulates axon growth. Whereas P2Y13 (through Gi) and P2X7 (through Ca2+) inhibit adenylate cyclase 5 (ADCY5), P2Y1 (through Gq) activates this enzyme. Changes in ADCY5 activity alter cAMP levels and protein kinase A activity, which subsequently leads to changes in signalling through the PI3K–Akt–GSK3 pathway. Through a carefully orchestrated interplay between the different types of receptors that converges on the same signalling module, neurons are thus able to precisely regulate the extent of axon growth in response to specific external stimuli.