“…In this way, the products of A 2A receptor activation are kept at low concentration under normal basal conditions and inactivation of striatal D 2 receptormediated neurotransmission (by administration of D 2 receptor antagonists, striatal dopamine depletion or genetic D 2 receptor inactivation) liberates A 2A receptormediated function from the strong D 2 receptor-mediated tonic inhibition. This results in a very significant increase in the striatal expression of c-Fos, Thr-34-phosphorylated DARPP-32, enkephalin, and neurotensin, which is partially counteracted by genetic inactivation or pharmacological blockade of A 2A receptors (Schiffman and Vanderhaeghen, 1993;Morelli et al, 1995;Pollack and Fink, 1995;Boegman and Vincent, 1996;Adams et al, 1997;Pinna et al, 1997Pinna et al, , 1999Richardson et al, 1997;Svenningsson et al, 1999aSvenningsson et al, , 2000Ward and Dorsa, 1999;Chen et al, 2000Chen et al, , 2001Zahniser et al, 2000;Dassesse et al, 2001;Ferré et al,. 2002;, see Section I.B.).…”