Fig. 4.

ATP-derived extracellular adenosine formed by CD73 activates A_2AR to control corticostriatal LTP. The high-frequency stimulation (HFS)–induced enhancement of the amplitude of population spikes (PS) – long-term potentiation (LTP) – recorded in corticostriatal synapses from wild-type (WT) mice slices was decreased in the presence of the CD73 inhibitor α,β-methylene ADP (AOPCP, 100 μM) (A), or of the selective A_2AR antagonist SCH58261 (50 nM) (B). C The effect of AOPCP was abrogated in slices from either CD73 knockout (KO) mice or A_2AR-KO mice. D Likewise, the effect of SCH58261 was also abrogated in slices from either CD73-KO or A_2AR-KO mice. This shows that CD73-derived extracellular adenosine selectively activates A_2AR to control corticostriatal LTP. Data are mean ± SEM of 4–6 experiments (number of different animals tested); *p < 0.05 using a Student’s t test with Welsh correction for comparison between two groups