PI3-kinase is required for CP-AMPAR-dependent long-term potentiation.

<p>(A) The specific PI3-kinase inhibitor LY294002 significantly attenuated NMDAR-dependent LTP induced by 2 trains of 100 Hz (as indicated by <i>arrow</i>) in GluR2+/+slices (vehicle, n = 6; LY294002, n = 5; <i>P</i><0.001). CP-AMPAR-dependent LTP elicited by 2 trains of 100 Hz (as indicated by <i>arrow</i>) in (B) GluR2−/−slices was also strongly suppressed in the presence of the structurally unrelated PI3K inhibitors LY294002 (vehicle, n = 5; D,L-AP5+LY294002, n = 5; <i>P</i><0.001) and wortmannin (vehicle, n = 5; D,L-AP5+wortmannin, n = 5; <i>P</i><0.001). (C) Summary graph of the means of the last 10 minutes of potentiation seen in LY294002 and wortmannin treatment studies. CP-AMPAR-dependent LTP recordings in GluR2 mutants involved the addition of 100 µM D,L-AP5 to perfusate 15 minutes prior to induction, ceasing at 5 minutes post-induction. 20 µM LY294002 and 1 µM wortmannin were added to ACSF perfusate 15–20 minutes prior to LTP induction up until 5 minutes post-induction. Error bars represent SEM. * denotes <i>P</i><0.05.</p>