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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
12                              Three different nicotinic agonists, ACh, nicotine, and dimethylphenylpip
13 easome activity was significantly blunted by nicotinic agonist administration in vivo.
14         Treatment of human kidney cells with nicotinic agonists, an NFkappaB inhibitor (Bay11), or a
15 ntary treatment of 17 beta-estradiol and the nicotinic agonist anabasine resulted in the translocatio
16                                          The nicotinic agonist anatoxin-a (AnTx) evoked monophasic [(
17 e) anabaseine (DMXB-A) is a partial alpha(7)-nicotinic agonist and can be taken orally.
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
22  cooperative fashion, not seen for classical nicotinic agonists and antagonists.
23  kinetics of whole-cell current responses to nicotinic agonists and are more sensitive to the beta2 s
24           Mutual occlusion of the effects of nicotinic agonists and ATP analogues were also observed
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
28  of GABA in the SpL can be regulated by both nicotinic agonists and mu opioids.
29 ctions between the hydrogen bond acceptor of nicotinic agonists and the complementary subunit backbon
30                                    An alpha7 nicotinic agonist appears to have positive effects on ne
31  of inward currents induced by 1 s pulses of nicotinic agonists, applied at 30 s intervals, gradually
32                                   The alpha7 nicotinic agonist AR-R17779 inhibited phosphorylation of
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
36           This indicates chronic exposure to nicotinic agonist as a potential pharmacological interve
37 nique binding mode for the cationic amine of nicotinic agonists at the alpha7 receptor.
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
40 hat physostigmine does not interact with the nicotinic agonist binding site.
41                           In the presence of nicotinic agonists, Ca2+i responses were transient.
42                     Spinal administration of nicotinic agonists can produce both hyperalgesic and ana
43 d by benzimidazole, macrocyclic lactone, and nicotinic agonist classes of anthelminthic drugs in the
44                                              Nicotinic agonists decreased evoked quantal output, but
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
47 no effect on sensitivity to the nonselective nicotinic agonist epibatidine.
48                                Occupation by nicotinic agonists, epibatidine and lobeline, and nicoti
49                               Even high-dose nicotinic agonists failed to overcome the inhibition by
50 human macrophages and suggest that selective nicotinic agonists for the alpha7nAChR might have therap
51 the nicotinic stimulation had ceased and the nicotinic agonist had been washed away.
52 n to slow channel closing in the presence of nicotinic agonists had a similar effect in the presence
53                           Clinical trials of nicotinic agonists have been mixed, underscoring the nee
54                     Pharmacophore models for nicotinic agonists have been proposed for four decades.
55                                  In general, nicotinic agonists have been shown to improve memory, an
56            Two types of structurally similar nicotinic agonists have very different biological and ph
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
59        The rank ordering of potencies of the nicotinic agonists in displacing (+/-)-[3H]epibatidine b
60 the potentially novel therapeutic effects of nicotinic agonists in patients with AD.
61                                              Nicotinic agonists induce peak whole-cell current respon
62                      The differences between nicotinic agonist induced catecholamine and serotonin re
63 ition within several hundred milliseconds of nicotinic agonist-induced fusion.
64 uced release of dopamine from PC12 cells and nicotinic agonist-induced hGH release from bovine adrena
65  activator, p25, led to a strong increase in nicotinic agonist-induced secretory responses.
66                                              Nicotinic agonist interactions with mollusk (Aplysia cal
67                             Similar to other nicotinic agonists, intrathecal (-)-epibatidine elicits
68 hese data suggest that nicotine or selective nicotinic agonists may represent a useful treatment stra
69     It has been shown that the non-selective nicotinic agonist nicotine has an influence on auditory
70                 Desensitizing effects of the nicotinic agonists nicotine and epibatidine were blocked
71                     The occlusive effects of nicotinic agonists on ATP-gated currents were blocked by
72 estigate the short- and long-term effects of nicotinic agonists on GABAergic transmission.
73 eta2-nAChRs with characteristic responses to nicotinic agonists or antagonists.
74 f currents elicited by low concentrations of nicotinic agonists, or, at higher concentrations, channe
75                          Carbachol and other nicotinic agonists produced marked increases in the freq
76                                    Classical nicotinic agonists show a 10-40-fold reduction in bindin
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
81                                    DMXB-A, a nicotinic agonist that activates alpha(7)-nicotinic rece
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
86                               The binding of nicotinic agonists to cell-surface BgtRs was highly coop
87 ve and contribute directly to the ability of nicotinic agonists to evoke GABA release in these region
88          Consistent with these observations, nicotinic agonist treatment significantly decreased rena
89                   These results suggest that nicotinic agonist treatments can ameliorate learning and
90                The rank order of potency for nicotinic agonists was as follows: epibatidine > nicotin
91                       The Ca(2+) response to nicotinic agonists was markedly prolonged in cells from
92 TP analogues on inward currents generated by nicotinic agonists were blocked by the P2X receptor anta

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