Increased ATP release and CD73-mediated adenosine A receptor activation mediate convulsion-associated neuronal damage and hippocampal dysfunction.

Extracellular ATP is a danger signal to the brain and contributes to neurodegeneration in animal models of Alzheimer's disease through its extracellular catabolism by CD73 to generate adenosine, bolstering the activation of adenosine A receptors (AR). Convulsive activity leads to increased ATP release, with the resulting morphological alterations being eliminated by AR blockade. However, it is not known if upon convulsions there is a CD73-mediated coupling between ATP release and AR overactivation, causing neurodegeneration.