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1 s were worsened by mecamylamine, a selective nicotinic antagonist.
2 ioning was attenuated by coadministration of nicotinic antagonist.
3 arinic antagonist and weakly attenuated by a nicotinic antagonist.
4 unctions and adenosine receptors, but not by nicotinic antagonists.
5 quency during inspiration was not altered by nicotinic antagonists.
6 or nicotinic agonists and lower affinity for nicotinic antagonists.
7 carinic or glutamate antagonists, but not by nicotinic antagonists.
8 onists, p = 0.01) for several noncompetitive nicotinic antagonists.
9   alpha-Conotoxins are two-disulfide-bridged nicotinic antagonists, 13-19 amino acids in length; kapp
10 s bisindolylmaleimide IV and V have far less nicotinic antagonist activity (IC(50) >1 microM); the ac
11 less frequent waves that could be blocked by nicotinic antagonists and had a characteristic postwave
12 g) and dihydro-beta-erythroidine (2 mg/kg) - nicotinic antagonists - and atropine (2 mg/kg) - a musca
13 maleimides I through III are the most potent nicotinic antagonists at the nicotinic cholinergic recep
14 ion was also inhibited by the muscarinic and nicotinic antagonists atropine and mecamylamine, respect
15                         Intrastriatally, the nicotinic antagonists blocked induction but not expressi
16  age of postnatal day 1 (P1) were blocked by nicotinic antagonists, but not by muscarinic or glutamat
17             In a dose-dependent fashion, the nicotinic antagonist catestatin blocked agonist desensit
18                                      Peptide nicotinic antagonists (catestatins, substance P) were fa
19 ion, making it the most neuronally selective nicotinic antagonist characterized thus far.
20                                          The nicotinic antagonists curare and dihydro-beta-erythroidi
21  blocked by the simultaneous addition of the nicotinic antagonist d-tubocurarine.
22                                            A nicotinic antagonist, d-tubocurarine chloride, completel
23 als, the inhibitory effect of muscarinic and nicotinic antagonists did not differ significantly.
24                      Further addition of the nicotinic antagonist dihydro-beta-erythroidine (DHbetaE)
25                     Focal application of the nicotinic antagonist dihydro-beta-erythroidine in an alp
26 educed in number or entirely absent when the nicotinic antagonist dihydro-beta-erythroidine was prese
27 antagonist atropine (0.1 microM), not by two nicotinic antagonists, dihydro-beta-erythroidine (10 mic
28                          Both muscarinic and nicotinic antagonists dose-dependently attenuated clonid
29                                     However, nicotinic antagonists, except hexamethonium, have compar
30                       In comparison to other nicotinic antagonists from Conus venoms, alphaS-RVIIIA e
31              alpha-Bungarotoxin, the classic nicotinic antagonist, has high specificity for muscle ty
32                                              Nicotinic antagonists have different effects on hair-cel
33                                          The nicotinic antagonists, however, blocked both the inducti
34 nists have been shown to improve memory, and nicotinic antagonists impair it.
35                 The rank order of potency of nicotinic antagonists in blocking the function of this a
36 irmed by blockade of the EPSPs or EPSCs with nicotinic antagonists, including DHbetaE, D-tubocurare,
37 e of the most potent noncompetitive neuronal nicotinic antagonists, indeed the most potent such antag
38 oxin MII, which is also a potent alpha3beta2 nicotinic antagonist, it is much less hydrophobic, and t
39 erent from the many conopeptides shown to be nicotinic antagonists; it is most similar in its general
40  of two sessions 2 hours after receiving the nicotinic antagonist mecamylamine (10 mg) or placebo ora
41 BAergic antagonists, but were blocked by the nicotinic antagonist mecamylamine (MEC).
42           Such responses were blocked by the nicotinic antagonist mecamylamine but not by the muscari
43  reduced attentional modulation, whereas the nicotinic antagonist mecamylamine had no systematic effe
44 ate antagonist kynurenic acid (KYNA) and the nicotinic antagonist mecamylamine hydrochloride (MCM) re
45 ted withdrawal by systemically injecting the nicotinic antagonist mecamylamine in mice chronically tr
46 nist methyllycaconitine or the non-selective nicotinic antagonist mecamylamine indicated that the eff
47 r chronic in ovo treatment with the neuronal nicotinic antagonist mecamylamine or the GABA receptor a
48                                          The nicotinic antagonist mecamylamine, 3 mg/kg, induced a sm
49 as abolished in the presence of the specific nicotinic antagonist mecamylamine, indicating that it wa
50 d by nicotine withdrawal precipitated by the nicotinic antagonist mecamylamine.
51                                              Nicotinic antagonists mecamylamine and dihydro-beta-eryt
52       When treated with an acute dose of the nicotinic antagonist, mecamylamine (0.5 mg/kg, sc), the
53       Pretreatment with the centrally acting nicotinic antagonist, mecamylamine (1 mg/kg), blocked ni
54 ne were blocked by pretreating rats with the nicotinic antagonist, mecamylamine.
55                        Local infusion of the nicotinic antagonist methyllycaconitine (MLA) to block a
56        Furthermore, coaddition of either the nicotinic antagonist methyllycaconitine citrate hydrate
57 ckade of this effect with either the alpha-7 nicotinic antagonist methyllycaconitine or the non-selec
58    Here, we report that the alpha7-selective nicotinic antagonist, methyllycaconitine (MLA), protects
59 inic agonists, epibatidine and lobeline, and nicotinic antagonists, methyllycaconitine, alpha-bungaro
60 n a manner that was in turn blocked with the nicotinic antagonist methyllyconitine (1 microM).
61                    In mouse striatal slices, nicotinic antagonists or depletion of endogenous acetylc
62                                        These nicotinic antagonist peptides from Conus are broadly div
63 dence indicated that each variant acted as a nicotinic antagonist: potency to inhibit secretion paral
64                                   In chicks, nicotinic antagonists such as alpha-bungarotoxin (alphaB
65 ype (thereby causing paralysis) and a second nicotinic antagonist targeted to the alpha3beta2 nAChR s
66 ging pattern in venomous predators, with one nicotinic antagonist targeted to the muscle subtype (the
67 hus, alphaS-RVIIIA defines a novel family of nicotinic antagonists within the S superfamily.

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