Tracking the A2A adenosine receptor

Background The A2A adenosine receptor has become a drug target in the treatment of Parkinson’s disease, psychotic behavior and dementia. In addition, targeted deletion of this receptor in mice leads to hypertension, increased platelet aggregation, male aggressiveness and decreased susceptibility to ischemic brain damage. The potential clinical relevance of this receptor is obvious. The A2A adenosine receptor, a prototypical GPCR, is known to signal via restricted collision coupling with Gs. In addition, it is able to stimulate MAP kinase/ERK in a Gs-independent way but dependent on the lipid microenvironment of the membrane. Hence, we characterized the mobility and the targeting of the A2A receptor in nerve cells.