Depression: a new enzyme AT play.
Helena Caria MartinsGerhard SchrattPublished in: EMBO reports (2020)
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.
Keyphrases
- signaling pathway
- depressive symptoms
- cerebral ischemia
- transcription factor
- genome wide
- white matter
- major depressive disorder
- early onset
- gene expression
- emergency department
- resting state
- brain injury
- epithelial mesenchymal transition
- escherichia coli
- pi k akt
- induced apoptosis
- cystic fibrosis
- pseudomonas aeruginosa
- adverse drug
- prefrontal cortex
- staphylococcus aureus
- subarachnoid hemorrhage