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1 restored the antinociceptive effects of the nicotinic agonist.
2 pinal excitatory amino acids released by the nicotinic agonist.
3 ics common with channel activity elicited by nicotinic agonists.
4 to modulate receptor activation by selected nicotinic agonists.
5 ding site that is distinct from the site for nicotinic agonists.
6 ponse data for epibatidine and several other nicotinic agonists.
7 hibit a high affinity for nicotine and other nicotinic agonists.
8 uid (aCSF) and found that application of the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium iod
9 of chromaffin vesicles was increased by the nicotinic agonist 1,1-dimethyl-4-phenyl-piperazinium iod
10 cell line are functional, and in response to nicotinic agonists, 86Rb+ efflux was increased to levels
11 bserved in 84% of patches (n = 118) when the nicotinic agonists acetylcholine (1-100 microM), carbamy
15 ntary treatment of 17 beta-estradiol and the nicotinic agonist anabasine resulted in the translocatio
18 t involved in specific interactions with the nicotinic agonist and that they affect the activation of
19 sensitive to simulation of egg-laying by the nicotinic agonist and was accompanied by a promoter-inde
20 we compared up-regulation by three different nicotinic agonists and a competitive antagonist of sever
21 or binding pose that differs from classical nicotinic agonists and antagonists and from the previous
23 kinetics of whole-cell current responses to nicotinic agonists and are more sensitive to the beta2 s
25 tameric oligomers in which binding sites for nicotinic agonists and competitive antagonists are found
26 be produced by a variety of drugs, including nicotinic agonists and competitive antagonists, but prev
27 competition studies reveal high affinity for nicotinic agonists and lower affinity for nicotinic anta
29 ctions between the hydrogen bond acceptor of nicotinic agonists and the complementary subunit backbon
31 of inward currents induced by 1 s pulses of nicotinic agonists, applied at 30 s intervals, gradually
33 he predominant effects of nicotine and other nicotinic agonists are related to desensitization of the
34 esults support previous work suggesting that nicotinic agonists are viable as treatments for adult AD
35 d that the neuroprotective actions of alpha7 nicotinic agonists arise from activation of receptors an
38 placebo-controlled double-blind trial of the nicotinic agonist AZD3480 (also termed TC-1734) at doses
39 oes not interfere with the occupation of the nicotinic agonist binding site by ACh, carbachol, or cho
43 d by benzimidazole, macrocyclic lactone, and nicotinic agonist classes of anthelminthic drugs in the
45 -2 (50 and 500 units/well, respectively), or nicotinic agonist dimethylphenylpiperazinium (10 microM,
46 lso showed higher seizure sensitivity to the nicotinic agonist epibatidine, but not to the GABA(A) re
50 human macrophages and suggest that selective nicotinic agonists for the alpha7nAChR might have therap
52 n to slow channel closing in the presence of nicotinic agonists had a similar effect in the presence
57 n-deficit/hyperactivity disorder (ADHD), and nicotinic agonists improve attention across preclinical
58 atidine has been shown to be the most potent nicotinic agonist in several neuronal nicotinic receptor
64 uced release of dopamine from PC12 cells and nicotinic agonist-induced hGH release from bovine adrena
68 hese data suggest that nicotine or selective nicotinic agonists may represent a useful treatment stra
74 f currents elicited by low concentrations of nicotinic agonists, or, at higher concentrations, channe
77 st action was specific to desensitization by nicotinic agonists, since catestatin did not block desen
78 igh levels of Ca2+, (ii) secretion caused by nicotinic agonist stimulation can be significantly enhan
79 Catecholamine secretion induced by other nicotinic agonists (such as epibatidine, anatoxin, or cy
80 ts on receptor activation by galantamine and nicotinic agonists, suggesting that the general features
82 ased on two disparate bound conformations of nicotinic agonists, thereby establishing an atypical con
83 th similar potency when triggered by several nicotinic agonists, though not by agents using other sec
84 opical application of either a muscarinic or nicotinic agonist to the exposed cortex, respectively, a
85 both proteasome activity and inflammation by nicotinic agonists to attenuate LPS-induced kidney injur
87 ve and contribute directly to the ability of nicotinic agonists to evoke GABA release in these region
92 TP analogues on inward currents generated by nicotinic agonists were blocked by the P2X receptor anta
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