1  reversibly blocked by the NMDA antagonist D-2-amino-5-phosphonovalerate (AP5) and the non-NMDA antag

2 s sensitive to the NMDA receptor antagonist, 2-amino-5-phosphonovalerate (AP5).

3 noxaline-2,3-dione (CNQX; 10 microM) and D,L-2-amino-5-phosphonovalerate (AP5; 100 microM).

4 ensitive to blockade by the NMDA antagonists 2-amino-5-phosphonovalerate (APV) and N-acetyl-aspartyl-

5                    The NMDA receptor blocker 2-amino-5-phosphonovalerate (APV) caused a slight reduct

6           In contrast, low concentrations of 2-amino-5-phosphonovalerate (APV) did not block either L

7                        Rats infused with D,L-2-amino-5-phosphonovalerate (APV) into the BLA or centra

8 The N-methyl-D-aspartate (NMDA) antagonist D-2-amino-5-phosphonovalerate (APV) was then applied, and

9 omote steroid production, we observed that D-2-amino-5-phosphonovalerate (APV), a competitive NMDAR a

10  presence of the NMDA receptor antagonist DL-2-amino-5-phosphonovalerate (APV).

11 ic N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovalerate (APV).

12                                  Infusion of 2-amino-5-phosphonovalerate (APV; 100 microM), an inhibi

13 ial training in the NMDAR antagonist APV (DL-2-amino-5-phosphonovalerate) blocked not only the condit

14  activation induced with TBS is resistant to 2-amino-5-phosphonovalerate, in contrast to that induced

15 ion of the NMDA-receptor antagonist AP5 (D,L-2-amino-5-phosphonovalerate) into the basolateral amygda

16              The NMDA receptor-antagonist dl-2-amino-5-phosphonovalerate significantly disrupted syna

17 so blocked by the NMDA receptor antagonist d-2-amino-5-phosphonovalerate, unlike granule cell mossy f