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 CD39, 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.