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ATP was particularly released at high stimulation intensities from purified striatal nerve terminals of mice, which were endowed with different ATP-P2 receptors (P2R), although P2R antagonists did not alter corticostriatal transmission or plasticity. Instead, ATP was extracellularly catabolized into adenosine through CD73 to activate adenosine A<jats:sub>2A<\/jats:sub> receptors (A<jats:sub>2A<\/jats:sub>R) modulating corticostriatal long-term potentiation (LTP) in mice. In the presymptomatic phase of a 6-hydroxydopamine rat model of PD, ATP release from striatal nerve terminals was increased and was responsible for a greater impact of CD73 and A<jats:sub>2A<\/jats:sub>R on corticostriatal LTP. These observations identify increased ATP release and ATP-derived formation of extracellular adenosine bolstering A<jats:sub>2A<\/jats:sub>R activation as a key pathway responsible for abnormal synaptic plasticity in circuits involved in the onset of PD motor symptoms. 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