Depression: a new enzyme AT play

Neuronal activity is the main contributor to the high‐energy demand of the human brain. ATP is needed for the maintenance of ionic gradients, neurotransmitter transport, and release, as well as the signaling pathways that follow activation of post‐synaptic receptors. The inability to maintain a high supply of ATP through tight regulatory mechanisms can, therefore, have severe consequences for brain function. In this issue of EMBO Reports , Cui et al [1] show that pharmacological inhibition or genetic inactivation of CD 39, an ectonucleotide tri(di)phosphohydrolase responsible for converting ATP into AMP , has antidepressant‐like effects by maintaining high extracellular ATP levels in the presence of stress.