ライフサイエンスコーパス: mecamylamine

1 wal precipitated by the nicotinic antagonist mecamylamine.

2 coronary effluent and this was prevented by mecamylamine.

3 s, which was antagonized by atropine but not mecamylamine.

4 onists, including DHbetaE, D-tubocurare, and mecamylamine.

5 ha3 AChRs were inhibited by hexamethonium or mecamylamine.

6 timulated 86Rb+ efflux, which was blocked by mecamylamine.

7 treating rats with the nicotinic antagonist, mecamylamine.

8 effects were blocked by the nAChR antagonist mecamylamine.

9 amine, and the nicotinic receptor antagonist mecamylamine.

10 the nicotinic acetylcholine receptor blocker mecamylamine.

11 artially blocked by either d-tubocurarine or mecamylamine.

12 ises were partially inhibited by atropine or mecamylamine.

13 -we found no effect of either scopolamine or mecamylamine.

14 amnestic effect of systemically administered mecamylamine.

15 ic acetylcholine receptor (nAChR) antagonist mecamylamine.

16 he potency of the non-competitive antagonist mecamylamine.

17 VEGF was suppressed by the nAChR antagonist mecamylamine.

18 s were generated for nicotine, bupropion and mecamylamine.

19 stration of the nicotine receptor antagonist mecamylamine.

20 ceptors, and were antagonized with 25 microm mecamylamine.

21 were unaffected by PPADS but were blocked by mecamylamine.

22 eally), a muscarinic receptor antagonist, or mecamylamine (0, 0.75, or 2.25 mg/kg, intraperitoneally)

23 h an acute dose of the nicotinic antagonist, mecamylamine (0.5 mg/kg, sc), the HFD animals responded

24 Systemically, mecamylamine (1 mg/kg) and dihydro-beta-erythroidine (2

25 Blockade of nicotinic receptors using mecamylamine (1 mg/kg) prevented both the behavioral and

26 h the centrally acting nicotinic antagonist, mecamylamine (1 mg/kg), blocked nicotine's effects, wher

27 ficantly depressed by a low concentration of mecamylamine (1 microM).

28 Sequential microinjections of mecamylamine (1 mM), an antagonist for nicotinic recepto

29 arinic (scopolamine, 5 microg) or nicotinic (mecamylamine, 1 microg) cholinergic antagonists administ

30 urs after receiving the nicotinic antagonist mecamylamine (10 mg) or placebo orally.

31 antagonized by the neuronal nAChR antagonist mecamylamine (10 microM).

32 thermore, the nicotinic receptor antagonist, mecamylamine (10 microM, n=13), eliminated the inhibitor

33 i.t. pretreatment with the nAChR antagonists mecamylamine (10 nmol)>MLA (100 nmol)>DHbetaE (50% with

34 rog/side), but not nicotinic antagonism with mecamylamine (10.0 microg/side), inhibited learning and

35 , n = 6) or a nicotinic receptor antagonist (mecamylamine, 10 mumol l(-1) , n = 6).

36 rs, but not by a nicotinic-receptor blocker (mecamylamine; 10 mum).

37 AChR) antagonists tubocurarine (100 microM), mecamylamine (100-500 microM) and dihydro-beta-erythroid

38 tine withdrawal syndrome was precipitated by mecamylamine (2 mg/kg, subcutaneous) in C57BL/6J nicotin

39 r the neuronal nicotinic receptor antagonist mecamylamine (3 microM).

40 The nicotinic antagonist mecamylamine, 3 mg/kg, induced a small increase in the t

41 The anxiogenic action of mecamylamine (30 and 100 ng) was most likely mediated by

42 c effects in conditions of moderate anxiety; mecamylamine (30 ng) was silent in these conditions, ind

43 ic acetylcholine receptor (nAChR) antagonist mecamylamine (5 micromol/kg, i.p.) but not by the periph

44 as blocked by subcutaneous administration of mecamylamine (50 mg/kg/d) by an osmotic pump.

45 nist alpha-bungarotoxin (100 nM), but not by mecamylamine (50 microM) or dihydro-beta-erythroidine (D

46 beta-erythroidine (DH beta E, 100 microM) or mecamylamine (50 microM) reduced EPSC amplitudes by 42 (

47 um (500 microM), decamethonium (500 microM), mecamylamine (50 microM), pentolinium (50 microM), adiph

48 Pretreatment with mecamylamine (6 micromol/kg s.c.), an nAChR blocker that

49 Pretreatment of the SFO with mecamylamine, a nicotinic receptor antagonist, had no ef

50 To test this, mecamylamine, a non-subtype selective nAChR antagonist,

51 Treatment of cells with mecamylamine, a noncompetitive antagonist, did not chang

52 e outcomes of intracranial microinfusions of mecamylamine, a nonselective nicotinic receptor antagoni

53 The motor defects were worsened by mecamylamine, a selective nicotinic antagonist.

54 the brain and indicate that epibatidine and mecamylamine act as 5-HT(3)R antagonists.

55 However, the noncompetitive nAChR antagonist mecamylamine acted as a potent competitive inhibitor of

56 tion was tested by a hippocampal infusion of mecamylamine alone or together with the DA D2 agonist qu

57 le APP, and APLP2, whereas co-treatment with mecamylamine (an antagonist of nicotinic acetylcholine r

58 The nAChR antagonist mecamylamine, an alpha7-nAChR subunit-specific antagonis

59 Furthermore, chronic application of mecamylamine, an antagonist of nAChRs, disrupts the gene

60 Mecamylamine, an nAChR antagonist, reversed the inhibiti

61 camylamine and alpha-bungarotoxin; (4) since mecamylamine and alpha-bungarotoxin are known to block n

62 pression in KCs, which could be abolished by mecamylamine and alpha-bungarotoxin with different effic

63 pression in KCs, which could be abolished by mecamylamine and alpha-bungarotoxin with different effic

64 ses, it is necessary to use a combination of mecamylamine and alpha-bungarotoxin; (4) since mecamylam

65 Mecamylamine and atropine, antagonists of nicotinic and

66 of responding, it was established that both mecamylamine and bupropion block nicotine's rate-reducin

67 halers, as well as pharmacotherapies such as mecamylamine and clonidine, serotonergic treatments such

68 ficantly higher concentrations compared with mecamylamine and conotoxin MII.

69 y and reversibly blocked by coapplication of mecamylamine and d-tubocurarine.

70 Nicotinic enhancement was inhibited by mecamylamine and DHbetaE, suggesting an important role f

71 Nicotinic antagonists mecamylamine and dihydro-beta-erythroidine inhibited res

72 These effects were blocked by mecamylamine and dihydro-beta-erythroidine, but not meth

73 yllycaconitine; noncompetitive antagonism by mecamylamine and eserine; and mixed antagonism by pancur

74 than that of nicotinic receptor antagonists (mecamylamine and hexamethonium).

75 Mecamylamine and kappa-bungarotoxin, which are cholinerg

76 ne as did the enantioselective separation of mecamylamine and methorphan.

77 While mecamylamine and prazosin had no effect, scopolamine, me

78 sing channel open times and burst durations, mecamylamine and tetracaine induced unique subconductanc

79 Mecamylamine and varenicline had similar potencies to bl

80 ccurs in the presence of the channel blocker mecamylamine and with the alpha4 mutant, which prevents

81 ha7nAChR antagonists, alpha-bungarotoxin and mecamylamine, and by specific siRNA-mediated STAT3 inhib

82 ow-sensitivity alpha4beta2, chlorisondamine, mecamylamine, and d-tubocurarine were, respectively, 100

83 found to be sensitive to alpha-bungarotoxin, mecamylamine, and dihydro-beta-erythroidine, indicating

84 ation of cholinergic neurons/fibers caused a mecamylamine- and atropine-sensitive inward current in p

85 NQX) and a nicotinic cholinergic (DHbetaE or mecamylamine) antagonist, or glycine and GABA receptor (

86 Mecamylamine antagonized this effect.

87 Epibatidine and mecamylamine are ligands used widely in the study of nic

88 ous studies that depended on epibatidine and mecamylamine as nAChR-specific ligands, in particular st

89 Displacement chromatography, with mecamylamine as the displacer, was used to verify that t

90 sence of bupropion and the nAChR antagonist, mecamylamine, as well as the ability of these drugs to a

91 The nAChR antagonist mecamylamine attenuated the cholinergic signals evoked b

92 entixol or the nicotinic receptor antagonist mecamylamine blocked NSIA in rats tolerant to the antino

93 Mecamylamine blocked rat alpha7 receptors weakly if co-a

94 ic acetylcholine receptor (nAChR) antagonist mecamylamine blocked the excitatory effect of systemic n

95 The nicotinic cholinergic antagonist mecamylamine blocks the haltere-to-flight motoneuron syn

96 ses were blocked by the nicotinic antagonist mecamylamine but not by the muscarinic antagonist atropi

97 (preferential alpha7-nAChR antagonists) and mecamylamine but was not affected by dihydro-beta-erythr

98 pha7 nAChRs, because it was blocked by 5 mum mecamylamine but was resistant to 100 nm alpha-bungaroto

99 rations of the nonselective nAChR antagonist mecamylamine completely and reversibly inhibited endothe

100 Topically administered mecamylamine could provide an appealing new treatment ap

101 Mecamylamine, d-tubocurarine, and hexamethonium blocked

102 Either pre- or post-formalin treatment with mecamylamine decreased phase 1 behaviors and significant

103 The channel blocker mecamylamine did not cause up-regulation of alpha3 beta2

104 Mecamylamine differentially blocked fast nicotinic trans

105 tant exposure to SS and the nAChR antagonist mecamylamine during gestation blocked the development of

106 ocurarine, hexamethonium, decamethonium, and mecamylamine either failed to up-regulate [3H]epibatidin

107 Whereas mecamylamine failed to reduce beta-endorphin analgesia o

108 Antagonizing nicotinic signaling with mecamylamine further aggravated acute and chronic inflam

109 e function of this alpha3/beta4 receptor was mecamylamine > d-tubocurarine > dihydro-beta-erythroidin

110 microM(-1) sec(-1), with a relative order of mecamylamine > dextromethorphan > or = ketamine > buprop

111 experience of the plus-maze pirenzepine and mecamylamine had anxiogenic effects in the dose range of

112 ne, diphenyl-acetoxy-N-methyl-piperidine and mecamylamine had no measurable effect on the CO2/H(+)-se

113 modulation, whereas the nicotinic antagonist mecamylamine had no systematic effect.

114 c acetylcholine receptor (nAChR) antagonist, mecamylamine, has been shown to be an effective add-on i

115 anner with the nonselective nAChR antagonist mecamylamine hydrochloride (0, 5, or 10 mg/d).

116 nic acid (KYNA) and the nicotinic antagonist mecamylamine hydrochloride (MCM) resulted in complete bl

117 temically injecting the nicotinic antagonist mecamylamine in mice chronically treated with nicotine.

118 In contrast to the significant effects of mecamylamine in the hippocampus, no effects were found a

119 investigates the neurochemical mechanism of mecamylamine in the regulation of extracellular serotoni

120 ne or the non-selective nicotinic antagonist mecamylamine indicated that the effect was mediated by n

121 resence of the specific nicotinic antagonist mecamylamine, indicating that it was mediated by keratin

122 jection of the nicotinic receptor antagonist mecamylamine induced behavioral symptoms of withdrawal m

123 uinpirole potentiated the amnestic effect of mecamylamine infused into the ventral hippocampus, where

124 evented by the nicotinic receptor antagonist mecamylamine, inhibitors of neuronal nitric oxide syntha

125 Mecamylamine injection triggered comparable withdrawal s

126 This implies that the unblocking rate for mecamylamine is much slower in C cells than B cells, and

127 ants (ka) for the noncompetitive inhibitors: mecamylamine, ketamine, bupropion, and dextromethorphan.

128 These results suggest that mecamylamine may block serotonin reuptake, the effect co

129 ic acetylcholine receptor (nAChR) antagonist mecamylamine (MCA) 30 min prior to nicotine challenge do

130 rodotoxin (TTX) and by the nAChR antagonists mecamylamine (MEC) and dihydro-beta-erythroidine (DHbeta

131 icantly attenuated by two nAChR antagonists, mecamylamine (MEC) and dihydro-beta-erythroidine (DHbeta

132 tively insensitive to the nAChR antagonists, mecamylamine (MEC) or dihydro-beta-erythroidine (DHbetaE

133 ade by the non-competitive nAChR antagonist, mecamylamine (Mec).

134 aining nAChR agonist cytisine and antagonist mecamylamine (MEC).

135 but were blocked by the nicotinic antagonist mecamylamine (MEC).

136 FC, and this evoked release was sensitive to mecamylamine (MEC).

137 caconitine (MLA)] or beta2*-nAChR-selective [mecamylamine (MEC)] antagonists but is prevented by coin

138 sing the anticholinergic antinicotinic agent mecamylamine (MECA) and antimuscarinic agent scopolamine

139 effluent (n = 8), but not in the presence of mecamylamine (n = 8).

140 3,3-tetramethylbicyclo[2.2.1]heptan-2-amine (mecamylamine), N-(2.6-dimethylphenylcarbamoylmethyl)trie

141 in tissues from P2X2+/+ mice were reduced by mecamylamine (nicotinic cholinergic receptor antagonist)

142 inergic antagonists scopolamine, atropine or mecamylamine, nor a series of non-cholinergic drugs, dia

143 Non-alpha7 nAChRs, blocked by 10 microM mecamylamine, occurred more frequently in the lateral rN

144 ct of in vivo administration of bupropion or mecamylamine on nicotine-stimulated (86)Rb(+) efflux was

145 Experiments with the nAChR channel blocker mecamylamine on P2X2-alpha6beta4 oocytes point to the lo

146 The effects of mecamylamine on rCBF were generally opposite to those of

147 itivity and spontaneous opening inhibited by mecamylamine) on alpha6beta4*-nAChR.

148 nic receptors, such as alpha-bungarotoxin or mecamylamine, only partially reversed these neuroprotect

149 ing this antagonism with the nAChR inhibitor mecamylamine or by RNAi knockdown of specific nAChR subu

150 was suppressed by the infusion of 50 mg/kg/d mecamylamine or by topical application 0.1 or 1% mecamyl

151 r infusion of alpha-bungarotoxin, but not by mecamylamine or dihydro-beta-erythroidine.

152 tment with the neuronal nicotinic antagonist mecamylamine or the GABA receptor agonist muscimol, agen

153 n-competitive non-selective nAChR antagonist mecamylamine or viral-mediated downregulation of the bet

154 for alpha7-containing receptors had little (mecamylamine) or no effect (dihydro-beta-erythroidine) o

155 y blocked by the antagonists d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine at concentrat

156 or carbamylcholine, but not d-tubocurarine, mecamylamine, or dihydro-beta-erythroidine, induced a 50

157 inhibitors (NCIs) of the nAChR (R)- and (S)-mecamylamine, phencylcidine, dextromethoprphan, and levo

158 type mice chronically treated with nicotine, mecamylamine precipitated withdrawal when microinjected

159 f nicotinic receptors, and it indicates that mecamylamine preferentially interacts with nicotinic rec

160 lar to the AT(4) antagonist, scopolamine and mecamylamine prevented acquisition of the water maze.

161 Despite these similarities, 8 microM mecamylamine reduced EPSC amplitude to a greater extent

162 l, but not the nicotinic receptor antagonist mecamylamine, reduced increases in mean arterial pressur

163 rinic and nicotinic antagonists atropine and mecamylamine, respectively, in dose- and time-dependent

164 Blocking of the nAChRs with mecamylamine resulted in reversible loss of cell-to-cell

165 antly reduced in rats administered 3.0 mg/kg mecamylamine (s.c.) 15 min prior to dissection compared

166 tylcholine recognition sites of nAChR (e.g., mecamylamine, scopolamine, N-methylspiperone and ketanse

167 avoidance behavior in lesioned animals in a mecamylamine-sensitive manner.

168 nd spatial Morris water task performances in mecamylamine-sensitive manners in bilaterally nucleus ba

169 e effects of repeated nicotine may depend on mecamylamine-sensitive nAChR stimulation.

170 obe component but not the training phase was mecamylamine-sensitive.

171 th cyclophosphamide or cyclophosphamide with mecamylamine suggested nuclear factor-kappa B activation

172 onist nicotine, the nicotinic ACh antagonist mecamylamine, the DA agonist apomorphine, or the DA anta

173 he ventral hippocampus, we infused nicotine, mecamylamine, the muscarinic ACh agonist pilocarpine, or

174 On the other hand, mecamylamine, the nicotinic cholinergic antagonist, fail

175 mylamine or by topical application 0.1 or 1% mecamylamine to the cornea.

176 We next used alpha-conotoxinMII and mecamylamine to understand the role of the alpha4beta2*

177 ubjective effects of smoking, was blocked by mecamylamine treatment.

178 We tested this by analyzing the effect of mecamylamine upon synaptic currents.

179 this was prevented when the nAChR antagonist mecamylamine was applied before or after nicotine.

180 The nAChR antagonist mecamylamine was only partially able to block the effect

181 effect of the nonselective nAChR antagonist mecamylamine was tested on human retinal and choroidal e

182 beta4 by hexamethonium and of alpha3beta2 by mecamylamine were 1.2 x 107 and 4.6 x 107 M-1 s-1, respe

183 hat bupropion shares behavioral effects with mecamylamine when administered in the presence of nicoti

184 This potentiation was blocked by mecamylamine, whereas galantamine had no effect on these