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1 cyano-7-nitroquinoxaline-2,3-dione) and AP5 (2-amino-5-phosphonopentanoic acid).
2 panoic acid] or NMDA antagonist d-AP5 [D-(-)-2-amino-5-phosphonopentanoic acid].
3 -elicited responses were blocked by D-AP5 (D-2-amino-5-phosphonopentanoic acid), a selective NMDA rec
4 y ionotropic glutamate receptor antagonists (2-amino-5-phosphonopentanoic acid and 6-cyano-7-nitro-qu
8 f the N-methyl-D-aspartate (NMDA) antagonist 2-amino-5-phosphonopentanoic acid (AP-5) into the amygda
9 processes, the NMDA receptor antagonist D, L-2-amino-5-phosphonopentanoic acid (AP-5) preferentially
10 osure of neurons to the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (AP-5) produced an inc
11 aspartate (NMDA), and were mimicked by (+/-)-2-amino-5-phosphonopentanoic acid (AP-5), a glutamate NM
12 ar infusion of the NMDA receptor antagonist, 2-amino-5-phosphonopentanoic acid (AP-5), provided that
14 o-7-nitroquinoxaline-2,3-dione (CNQX) and DL-2-amino-5-phosphonopentanoic acid (AP-5; 30 pmol each) a
15 DA receptors in the core with the antagonist 2-amino-5-phosphonopentanoic acid (AP-5; 5 nmol) abolish
16 itive N-methyl-D-aspartate (NMDA) antagonist 2-amino-5-phosphonopentanoic acid (AP-5; 5 nmol/0.5 micr
17 P < 0.01), but not by the NMDA antagonist dl-2-amino-5-phosphonopentanoic acid (AP-5; n = 6, P = 0.28
18 al training, the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5) or an Arc antise
19 te receptors, because it is antagonized by D-2-amino-5-phosphonopentanoic acid (AP5) or extracellular
20 pounds N-methyl-d-aspartate (NMDA) and d-(-)-2-amino-5-phosphonopentanoic acid (AP5), acts as positiv
21 attenuated by the co-administration of (+/-)-2-amino-5-phosphonopentanoic acid (AP5), an NMDA antagon
26 o-5-phosphonovaleric acid (APV; 50 mM) or DL-2-amino-5-phosphonopentanoic acid (AP5, 20 mM) block myo
27 the specific N-methyl-D-aspartate antagonist 2-amino-5-phosphonopentanoic acid (AP5, 50 or 100 microM
28 The effects of infusing the NMDA antagonist 2-amino-5-phosphonopentanoic acid (AP5; 100 microM), neu
30 -methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (APV) or the CaM kinas
31 ry postsynaptic amino acid antagonists D-(-)-2-amino-5-phosphonopentanoic acid (APV) plus 6,7-dinitro
32 to the neurotransmitter receptor blockers D-2-amino-5-phosphonopentanoic acid, bicuculline, 6-cyano-
33 d by NMDA and blocked by an NMDA antagonist, 2-amino-5-phosphonopentanoic acid, but not by the AMPA a
35 he nonselective NMDA receptor antagonist d,l-2-amino-5-phosphonopentanoic acid (d,l-AP5) significantl
36 ed by injection of the NMDAR antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP-5) in the L5-DRG
38 tructures reveal that the antagonists, D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5) and 1-(phenant
39 ing requirement for glycine, antagonism by D-2-amino-5-phosphonopentanoic acid (D-AP5) and 7-chloroky
41 ast, treatment with the NMDA antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) greatly increa
42 eating, the NMDA receptor antagonists d-(-)-2-amino-5-phosphonopentanoic acid (D-AP5) or 7-chlorokyn
43 form of the NMDA receptor antagonist, D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5) to block the a
44 ections of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) to the goldfis
45 -quinoxaline-7-sulphonamide (NBQX) and D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5), a small EPSC
46 D-aspartate (NMDA) receptor antagonists D(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 50 microM) had
47 ished by the NMDA receptor antagonist, D-(-)-2-amino-5-phosphonopentanoic acid (D-AP5; 50 microM).
48 nfusion of the NMDA receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-APV) into the basol
49 the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid did not alter the perc
51 agonist at NMDA receptors (20-50 microM D(-)-2-amino-5-phosphonopentanoic acid; EPSP amplitude 109%;
52 0)] by suspending the competitive antagonist 2-amino-5-phosphonopentanoic acid in the slow release pl
53 ptor antagonism with microinjections of AP5 (2-amino-5-phosphonopentanoic acid) into iVRG decreased T
54 tions of a glutamate antagonist cocktail (DL-2-amino-5- phosphonopentanoic acid lithium salt [AP-5] +
55 D-aspartate receptor antagonists MK-801/D(-)-2-amino-5-phosphonopentanoic acid or by depletion of glu
56 results and did not observe glutamate, d-(-)-2-amino-5-phosphonopentanoic acid, or N-methyl-d-asparta
57 ial NMDAR antagonism by low concentration DL-2-Amino-5-phosphonopentanoic acid rescued a basal LTP de
58 N-methyl-d-aspartate (NMDA) antagonist [D(-)-2-amino-5-phosphonopentanoic acid], suggesting that preg