“…This functional antagonism is the basis for the development of A 2A R antagonists as a promising nondopaminergic pharmacological therapy for Parkinson's disease , whereas A 2A R agonists have been proposed as potential therapeutic agents for schizophrenia (Ferre, 1997) and other psychotic disorders (Fredholm et al, 2005). However, contrary to the antagonistic A 2A R-D 2 R interaction model in the striatum and certain pharmacological data (Filip et al, 2006), genetic inactivation of A 2A Rs either globally or specifically in forebrain region attenuates, rather than enhances, the psychostimulant effects of cocaine (Chen et al, 2000), amphetamine (Chen et al, 2003;Bastia et al, 2005), or L-dopa (Fredduzzi et al, 2002;Xiao et al, 2006). These observations suggest that the activation of A 2A Rs in extrastriatal cells may oppose postsynaptic A 2A R function in striatopallidal neurons on the modulation of psychomotor activity.…”