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1 nt receptor approached M2 sensitivity toward gallamine.
2 to M(1) significantly increased affinity for gallamine.
3 lscopolamine and allosterically inhibited by gallamine.
4 t and is not part of the allosteric site for gallamine.
5 high doses of any of the ligands used except gallamine.
6 ists and antagonists such as pilocarpine and gallamine.
7 n-2-yl]phenoxy]heptyl]-1,2-oxazole (W84) and gallamine.
8 ation of tracheas in the presence/absence of gallamine.
9 8% by pirenzepine (10(-5) M), 69% +/- 14% by gallamine (10(-5) M), and 72% +/- 11% by 4-DAMP mustard
11 enic effects in the dose range of 30-300 ng; gallamine (100 and 300 ng) was without significant effec
17 obidoxime reversed the allosteric effects of gallamine and other ligands suggested that they neverthe
19 rsibly to a site distinct from that to which gallamine and strychnine bind: in contrast, PG987 seems
21 and M2 receptor antagonists, pirenzepine and gallamine, and the nicotinic receptor antagonist mecamyl
22 residues in the o3 region of M(1) and M(4); gallamine appears to interact with both regions of the M
23 e of M(1) (LAGQ) reduced the affinity toward gallamine, as reported previously by others; the convers
24 by the peripheral site ligands propidium and gallamine at low concentrations of either acetylthiochol
25 ligands, AC-42, and the allosteric modulator gallamine behaved as competitors of para-LRB-AC42 bindin
26 l of the above mutations are consistent with gallamine binding with a similar orientation at each sub
28 tested for the pair of agents metocurine and gallamine by determining the ability of a mixture of age
29 potency (atropine > pirenzepine = 4-DAMP >> gallamine) consistent with regulation by M1, rather than
30 studies reported that the M2 selectivity of gallamine depended largely on the EDGE (172-175) sequenc
31 at both AC-42 and the prototypical modulator gallamine failed to fully inhibit specific [(3)H]NMS bin
32 stent with the idea that both metocurine and gallamine have a high affinity for the same site on the
33 type-selective antagonists pirenzepine (M1), gallamine (M2), and 4-4-diphenylacetoxy-N-(2-chloroethyl
34 elective), pirenzepine and telenzepine (M1), gallamine (M2), and 4-diphenylacetoxy-N-methylpiperidine
35 g neuromuscular blocking agents (atracurium, gallamine, metocurine, and pancuronium) to act as compet
36 (1 mg/kg) did not alter the effect of either gallamine or pilocarpine, thus in pathogen free animals
37 mutations had no effect on the potencies of gallamine or W84 and even increased the potency of THA.
38 described mAChR allosteric compounds such as gallamine or WIN 62,577 (17-beta-hydroxy-17-alpha-ethyny
39 ckade of neuronal M2 muscarinic receptors by gallamine potentiated vagally induced bronchoconstrictio
40 he dominant residue in the o3/TM7 region for gallamine's high potency, although 419Asn can substitute
42 f M2 receptors), indomethacin prevented both gallamine's potentiation and pilocarpine's inhibition of
45 domains, overlapping or not with the classic gallamine site, but distinct from the allosteric indoloc
46 > N resulted in an increased affinity toward gallamine, suggesting that the asparagine residue at M(2
49 g-1 I.P., then 10 mg kg-1 I.V. as required), gallamine-triethiodide-treated (10 mg kg-1 I.V., then 2-
50 osteric binding parameters of the modulators gallamine, W84, and tetrahydroaminoacridine (THA) at M2
51 ion of M(5) markedly reduced affinity toward gallamine, whereas substitution into M(4) had no effect.
52 ociated with slightly higher affinity toward gallamine, whereas the valine and lysine residues of M(5
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