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In the present study, A<jats:sub>2A<\/jats:sub>R messenger RNA (mRNA) and receptor\u2010specific binding in the brain of 1\u2010methyl\u20104\u2010phenyl\u20101,2,3,6\u2010tetrahydropyridine (MPTP) monkeys were studied after treatment with<jats:sc>L<\/jats:sc>\u2010DOPA and a selective NR1A\/2B NMDA receptor antagonist, CI\u20101041. Four MPTP monkeys received<jats:sc>L<\/jats:sc>\u2010DOPA\/benserazide and all developed dyskinesias, whereas among the four MPTP monkeys who additionally received CI\u20101041, only one developed mild dyskinesias. Four normal monkeys and four MPTP\u2010treated monkeys were also studied. All MPTP monkeys had similar striatal dopamine (DA) denervation. A<jats:sub>2A<\/jats:sub>R mRNA levels, measured by in situ hybridization, were increased in the rostral lateral caudate and putamen of saline\u2010treated MPTP monkeys as well as in the caudal lateral and medial putamen when compared with those of controls. A<jats:sub>2A<\/jats:sub>R mRNA levels remained elevated in the rostral caudate and putamen of<jats:sc>L<\/jats:sc>\u2010DOPA\u2010treated MPTP monkeys when compared with those of controls. A<jats:sub>2A<\/jats:sub>R mRNA levels of<jats:sc>L<\/jats:sc>\u2010DOPA + CI\u20101041\u2010treated monkeys were at control levels and decreased in the lateral rostral caudate and caudal putamen when compared with those of<jats:sc>L<\/jats:sc>\u2010DOPA\u2010treated and saline\u2010treated MPTP monkeys respectively. No change was measured in the caudal medial putamen and caudate nucleus. A<jats:sub>2A<\/jats:sub>Rs labeled by autoradiography with [<jats:sup>3<\/jats:sup>H]SCH\u201058261 had lower level in the<jats:sc>L<\/jats:sc>\u2010DOPA + CI\u20101041\u2010treated MPTP monkeys compared with saline\u2010 or<jats:sc>L<\/jats:sc>\u2010DOPA\u2010treated MPTP and control monkeys in the rostral lateral and medial caudate and the putamen. No effect of lesion or<jats:sc>L<\/jats:sc>\u2010DOPA treatment was measured on [<jats:sup>3<\/jats:sup>H]SCH\u201058261\u2010specific binding. These findings suggest that blockade of NMDA receptors could prevent the development of dyskinesias by altering A<jats:sub>2A<\/jats:sub>Rs. 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