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1 oxicity could be prevented with memantine, a glutamate antagonist.
2 hippocampal areas during bath application of glutamate antagonists.
4 hich are blocked following co-injection with glutamate antagonists; 3) that peripheral injection of S
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
11 r, was completely inhibited by muscarinic or glutamate antagonists, but not by nicotinic antagonists.
13 nstrated that NMDA open channel blockade and glutamate antagonists can provide full neuroprotection a
15 pretreatments with intra-VP injections of a glutamate antagonist cocktail (DL-2-amino-5- phosphonope
16 and latency were unchanged by application of glutamate antagonists, consistent with a monosynaptic co
18 be stimulated with low voltages, wash out of glutamate antagonists did not reveal evoked glutamate cu
20 d synaptic properties and actions of GABA or glutamate antagonists during ETX in IC dorsal cortex (IC
21 h) with local injections of GABA agonists or glutamate antagonists elicits an intense, but specific,
22 conditioned stimulus while injections of the glutamate antagonist gamma-d-glutamylglycine were admini
23 ecome less clear as multiple human trials of glutamate antagonists have failed to show effective neur
24 and by inhibiting HC light responses with a glutamate antagonist, indicating that they were caused b
26 t if preceded by a 10-day treatment with the glutamate antagonists injected unilaterally once daily i
27 l microinjections of lidocaine, muscimol, or glutamate antagonists into the pTRG inhibited completely
28 One of the major tenets in the chemistry of glutamate antagonists is that the incorporation of phosp
29 ary evidence suggests that administering the glutamate antagonist ketamine with ECT might alleviate c
31 gic receptors, because co-application of the glutamate antagonist kynurenic acid (KYNA) and the nicot
32 In each case, infusion of the ionotropic glutamate antagonist kynurenic acid blocked the VTA dopa
38 e inputs as it was blocked by the ionotropic glutamate antagonist NBQX, but independent of visceral a
40 full expression of ethambutol toxicity, and glutamate antagonists prevent ethambutol-mediated cell l
41 )-2-amino-7-phosphonoheptanoic acid (D-AP7), glutamate antagonists, reduced the inhibition of neurona
44 itudes, but not frequency, of sPFPs, whereas glutamate antagonists suppressed frequency but not ampli
45 g the NAc by blocking excitatory inputs with glutamate antagonists, we dissociated core and shell con
47 als could be achieved by using injections of glutamate antagonists, which reduce, but do not eliminat
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