ライフサイエンスコーパス: D-APV

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1 nist, D-(-)-2-amino-5-phosphonovaleric acid (D-APV).

2 ntagonist D-2-amino-5-phosphonovaleric acid (D-APV).

3 by either 25 microM bicuculline or 25 microM D-APV.

4 sensitivity to the glutamate-site antagonist d-APV.

5 dritic spines are reduced in the presence of D-APV.

6 ate receptor antagonists (NBQX, 5 microm and D-APV, 10 microm), electrical stimulation of the ipsilat

7 e of EAA receptor antagonists (40-100 microM D-APV+20 microM CNQX, or 5 mM kynurenic acid) plus the G

8 esence of D-2-amino-5-phosphonovaleric acid (D-APV, 50 microM), 6-cyano-7-nitro-quinoxaline-2,3-dione

9 nce of D(-)-2-amino-5-phosphonovaleric acid (D-APV), an NMDA-site antagonist.

10 ed by Panx1, and the combined application of D-APV and (10)panx (a Panx1 blocker) inhibited AD curren

11 Importantly, the NMDAR antagonists, D-APV and R-CPP, attenuated AD currents carried by Panx1

12 onist D-(-)-2-amino-5-phosphonovaleric acid (D-APV) as well as the broad-spectrum glutamate receptor

13 "HVc" EP-SPs were relatively insensitive to D-APV but almost completely abolished by CNQX.

14 In contrast, infusion of d-APV immediately after the memory reactivation session

15 the non-subunit-selective NMDAR antagonist, D-APV, in organotypic hippocampal slice cultures.

16 nist D(-)-2-amino-5-phosphonopentanoic acid (D-APV) into the basolateral amygdala before a memory rea

17 that the reconsolidation-impairing effect of D-APV is correlated with downstream reductions in expres

18 wing the application of an NMDAR antagonist, D-APV, onto the cortical surface.

19 limited either by moderate concentrations of D-APV or by voltage clamping cells at negative membrane

20 ical blockade of NMDA receptor channels with D-APV or chelation of intracellular calcium ions with EG

21 -96365, but not the NMDA receptor antagonist d-APV, prevented BDNF-induced GluA1 surface expression a

22 gonist, 5,7-dichlorokynurenate (DCK) or with D-APV, respectively, did not result in agonist-induced o

23 cts could not be prevented by application of d-APV, the glutamate-site NMDAR antagonist, and were sti

24 Chronic NVP-AAM077 or D-APV treatment had little effect on these measures.

25 In contrast, the D-APV treatment of DAKO brains did not augment NR2A labe

26 ytochemistry revealed that, as expected, the D-APV treatment of wild-type (WT) mouse cortex increased

27 ally recorded CF responses were reduced when D-APV was bath applied.

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