ライフサイエンスコーパス: mecamylamine

1 and were insensitive to the channel blocker mecamylamine.

2 accumbal dopamine modulation by nicotine and 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 coronary effluent and this was prevented by mecamylamine.

11 artially blocked by either d-tubocurarine or mecamylamine.

12 ises were partially inhibited by atropine or mecamylamine.

13 amnestic effect of systemically administered mecamylamine.

14 the nicotinic acetylcholine receptor blocker mecamylamine.

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

16 or low glucose, acetylcholine (ACh), and/or mecamylamine.

17 he potency of the non-competitive antagonist mecamylamine.

18 g protracted bursts, even in the presence of mecamylamine.

19 VEGF was suppressed by the nAChR antagonist mecamylamine.

20 s were generated for nicotine, bupropion and mecamylamine.

21 wal precipitated by the nicotinic antagonist mecamylamine.

22 stration of the nicotine receptor antagonist mecamylamine.

23 ic acetylcholine receptor (nAChR) antagonist mecamylamine.

24 ceptors, and were antagonized with 25 microm mecamylamine.

25 were unaffected by PPADS but were blocked by mecamylamine.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 Mecamylamine, an nAChR antagonist, reversed the inhibiti

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

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

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

68 Mecamylamine and atropine, antagonists of nicotinic and

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

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

71 ficantly higher concentrations compared with mecamylamine and conotoxin MII.

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

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

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

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

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

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

78 Mecamylamine and kappa-bungarotoxin, which are cholinerg

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

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

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

82 Mecamylamine and varenicline had similar potencies to bl

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

84 3) surgical vagotomy, 4) nicotinic receptor (mecamylamine) and muscarinic receptor (AQ-RA 741) blocka

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

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

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

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

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

90 Mecamylamine antagonized this effect.

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

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

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

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

95 The nAChR antagonist mecamylamine attenuated the cholinergic signals evoked b

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

97 Mecamylamine blocked rat alpha7 receptors weakly if co-a

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

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

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

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

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

103 insensitive to the noncompetitive antagonist mecamylamine compared with GAT107 responses.

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

105 Topically administered mecamylamine could provide an appealing new treatment ap

106 Mecamylamine, d-tubocurarine, and hexamethonium blocked

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

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

109 Mecamylamine differentially blocked fast nicotinic trans

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

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

112 Whereas mecamylamine failed to reduce beta-endorphin analgesia o

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

130 Mecamylamine injection triggered comparable withdrawal s

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

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

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

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

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

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

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

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

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

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

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

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

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

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

145 3,3-tetramethylbicyclo[2.2.1]heptan-2-amine (mecamylamine), N-(2.6-dimethylphenylcarbamoylmethyl)trie

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 Mecamylamine-precipitated withdrawal significantly incre

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

191 lamine and the nicotinic receptor antagonist mecamylamine, while recording single cells in parafoveal