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. Author manuscript; available in PMC: 2011 Feb 1.
Published in final edited form as: Nat Neurosci. 2010 Jul 4;13(8):958–966. doi: 10.1038/nn.2592

Figure 7. Push-pull modulation of NMDARs by D2Rs and A2ARs is dependent on PKA activity.

Figure 7

(a) Uncaging-evoked NMDAR-mediated uEPSCs (upper traces) andΔCasp (lower traces), recorded as in Fig. 4a. Mean (black solid lines) and mean ± SEM (dark gray shaded regions) are shown for responses evoked in the presence of the PKA antagonist PKI(14-22) alone (1st column, n=21), PKI(14-22) + quinpirole (2nd column, n=20), the A2AR agonist CGS-21680 alone (n=16, 3rd column) or CGS-21680 + quinpirole (4th column, n=15). Medium gray and light gray shaded regions indicate the mean ± SEM responses under control and quinpirole conditions, respectively, reproduced from Fig. 4a for comparison.

(b) Population data for peak uEPSC (left) andΔCasp (right) are shown for the conditions illustrated in (a). Also shown are the population data for the PKA antagonist H89, the NR2B subunit-containing NMDAR antagonist ifenprodil, the A2AR antagonist SCH-58261, and SCH-58261 + quinpirole.

* indicates a significant difference compared to control (p<0.05).