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1  to their performance under normal saline or methylscopolamine.
2 on of binding sites for the antagonist [3H]N-methylscopolamine.
3 asured with the hydrophilic antagonist [3H]N-methylscopolamine.
4 e of action of AC-42 was obtained in [(3)H]N-methylscopolamine ([(3)H]NMS) binding studies, in that b
5 entration of ACh required to inhibit [(3)H]N-methylscopolamine ([(3)H]NMS) binding to M1, left-shifti
6 ors and can slow the dissociation of [(3)H]N-methylscopolamine ([(3)H]NMS) from these receptors.
7      After short preincubations with N-[(3)H]methylscopolamine ([(3)H]NMS) or R(-)-[(3)H]quinuclidiny
8 r toxins that inhibit the binding of [(3)H]N-methylscopolamine ([(3)H]NMS) to cloned M2 receptors.
9 3N by BR384 was competitively inhibited by N-methylscopolamine and allosterically inhibited by gallam
10 nalogues, were positively cooperative with N-methylscopolamine at least at one other subtype.
11             Binding experiments with [(3)H]N-methylscopolamine at the M(1), M(2), M(3), and M(4) mACh
12 ositively cooperative with the antagonist, N-methylscopolamine, at m2 receptors and, in the case of t
13 t affinity (K(i) = 2.24 muM) for the [(3)H]N-methylscopolamine binding site on the M5 receptor, is po
14 ompetition kinetics using whole-cell [(3)H]N-methylscopolamine binding, validating this approach as a
15                           [(3)H]NMS ([(3)H]N-methylscopolamine) binding experiments confirm that LY21
16 ne completely inhibited the binding of [3H]N-methylscopolamine, but yielded a shallow competition iso
17 phate (GMP-PNP) on the inhibition of N-[(3)H]methylscopolamine by the agonist oxotremorine-M.
18 ype non-selective antagonists atropine and N-methylscopolamine did not.
19 ic agents modulate the dissociation of [3H]N-methylscopolamine from M2/M5 chimeric and point-mutated
20 ted the learning of negative patterning, but methylscopolamine had no effect.
21 rug treatments (lithium chloride infusion or methylscopolamine injection).
22 -substituted analogues of brucine with [3H]N-methylscopolamine (NMS) and unlabeled acetylcholine at m
23 ties with acetylcholine and the antagonist N-methylscopolamine (NMS) at M(1)minus signM(4) receptors
24 agonists quinuclidinyl benzilate (QNB) and N-methylscopolamine (NMS) bind to the binding pocket of th
25 f kinetics of the radiolabeled antagonists N-methylscopolamine (NMS) in the presence of methoctramine
26                   Injections of scopolamine, methylscopolamine, or saline were started at the same ti
27                                   In [(3)H]N-methylscopolamine radioligand dissociation assays, appro
28 in a significant reduction in apparent N-[3H]methylscopolamine saturation binding affinity in intact
29 en alcuronium and the classical antagonist N-methylscopolamine that is characteristic of M(5) (these
30 ecreased binding of orthosteric antagonist N-methylscopolamine to human M1- and M2-mAChRs, and increa
31 mum M(1)-blockade, the binding of 1 nM [3H]N-methylscopolamine to striatal membranes was reduced by o
32        Some of the variants that bound [3H]N-methylscopolamine underwent small changes in their affin
33 nic receptor antagonist, atropine, and [3H]N-methylscopolamine was investigated, however, ATP was una

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