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1 oxicity could be prevented with memantine, a glutamate antagonist.
2 hippocampal areas during bath application of glutamate antagonists.
3                The EPSCs were blocked by the glutamate antagonist 2,3-dihydroxy-6-nitro-7-sulfonyl-be
4 hich are blocked following co-injection with glutamate antagonists; 3) that peripheral injection of S
5               Intraolivary injections of the glutamate antagonists 6-cyano-7-nitroquinoxaline-2,3-dio
6 th species, hyperpolarizing HCs by puffing a glutamate antagonist, 6,7-dinitro-quinoxaline-2,3-dione
7 fore unexplained short therapeutic window of glutamate antagonists after brain injury and support a p
8                              The competitive glutamate antagonists AP5 and GluN2B-selective inhibitor
9                                              Glutamate antagonists are considered major drug candidat
10                                         This glutamate antagonist blocks AMPA and kainate receptors a
11 r, was completely inhibited by muscarinic or glutamate antagonists, but not by nicotinic antagonists.
12 e and a phospholipase-D coupled metabotropic glutamate antagonist can abolish firing during static st
13                                              Glutamate antagonists can block ganglion cell death due
14 nstrated that NMDA open channel blockade and glutamate antagonists can provide full neuroprotection a
15 ese up states were completely blocked by the glutamate antagonist CNQX.
16  pretreatments with intra-VP injections of a glutamate antagonist cocktail (DL-2-amino-5- phosphonope
17 and latency were unchanged by application of glutamate antagonists, consistent with a monosynaptic co
18                                   The potent glutamate antagonists, CPP and CGP40116 and dizocilpine
19 be stimulated with low voltages, wash out of glutamate antagonists did not reveal evoked glutamate cu
20                                 In both, the glutamate antagonist dizocilpine (MK-801) reduced the sw
21      Microinjections in nucleus accumbens of glutamate antagonist, DNQX, which might suppress local n
22 d synaptic properties and actions of GABA or glutamate antagonists during ETX in IC dorsal cortex (IC
23 h) with local injections of GABA agonists or glutamate antagonists elicits an intense, but specific,
24 conditioned stimulus while injections of the glutamate antagonist gamma-d-glutamylglycine were admini
25 ecome less clear as multiple human trials of glutamate antagonists have failed to show effective neur
26  and by inhibiting HC light responses with a glutamate antagonist, indicating that they were caused b
27                   Furthermore, intrastriatal glutamate antagonist infusions increased the occurrence
28 t if preceded by a 10-day treatment with the glutamate antagonists injected unilaterally once daily i
29 l microinjections of lidocaine, muscimol, or glutamate antagonists into the pTRG inhibited completely
30  One of the major tenets in the chemistry of glutamate antagonists is that the incorporation of phosp
31 ary evidence suggests that administering the glutamate antagonist ketamine with ECT might alleviate c
32                        Microinjection of the glutamate antagonist kynurenate into the CVLM eliminated
33 gic receptors, because co-application of the glutamate antagonist kynurenic acid (KYNA) and the nicot
34     In each case, infusion of the ionotropic glutamate antagonist kynurenic acid blocked the VTA dopa
35                        Microinjection of the glutamate antagonist, kynurenic acid (50 nl; 100 mM) int
36                                              Glutamate antagonists may be useful in limiting the side
37                       Pretreatment with NMDA glutamate antagonists MK-801 or CPP dose-dependently att
38                                          The glutamate antagonists MK801 and NBQX blocked the glutama
39 e D(1) antagonist SCH 23390(1 microg) or the glutamate antagonist NBQX (0.1 microg).
40 e inputs as it was blocked by the ionotropic glutamate antagonist NBQX, but independent of visceral a
41 TS TH-EGFP neurons, an effect blocked by the glutamate antagonist NBQX.
42  full expression of ethambutol toxicity, and glutamate antagonists prevent ethambutol-mediated cell l
43 )-2-amino-7-phosphonoheptanoic acid (D-AP7), glutamate antagonists, reduced the inhibition of neurona
44 ng the most potent broad spectrum ionotropic glutamate antagonists reported.
45                               A metabotropic glutamate antagonist, (RS)-alpha-cyclopropyl-4-phosphono
46 itudes, but not frequency, of sPFPs, whereas glutamate antagonists suppressed frequency but not ampli
47 g the NAc by blocking excitatory inputs with glutamate antagonists, we dissociated core and shell con
48                           Microinjections of glutamate antagonists were made bilaterally into the NTS
49 als could be achieved by using injections of glutamate antagonists, which reduce, but do not eliminat
50                            Kynurenic acid, a glutamate antagonist with preference for the glycine sit