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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
16 age of postnatal day 1 (P1) were blocked by nicotinic antagonists, but not by muscarinic or glutamat
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
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
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
49 as abolished in the presence of the specific nicotinic antagonist mecamylamine, indicating that it wa
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
63 dence indicated that each variant acted as a nicotinic antagonist: potency to inhibit secretion paral
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
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