ライフサイエンスコーパス: ACh receptor

1 is a low-efficacy agonist of the muscle-type ACh receptor.

2 endplate potential and no deficiency of the ACh receptor.

3 abolished the nefiracetam stimulation of the ACh receptor.

4 echanism of action ibogaine at the nicotinic ACh receptor.

5 ights into the structure and function of the ACh receptor.

6 to supplement influx through the ionotropic ACh receptor.

7 le conformation may never be attained by the ACh receptor.

8 uiring activation of glutamate and nicotinic ACh receptors.

9 only used to immunolocalize alpha7 nicotinic ACh receptors.

10 o the extracellular domains of the nicotinic ACh receptors.

11 reveal the basis for agonist recognition by ACh receptors.

12 ebrafish to mutant fish lacking postsynaptic ACh receptors.

13 regulating surface trafficking of functional ACh receptors.

14 cle that involves activation of postsynaptic ACh receptors.

15 approximately 10-fold lower than those of m3 Ach receptors.

16 ting that it was mediated by M(2) muscarinic ACh receptors.

17 fecundity via helminth-expressed muscarinic ACh receptors.

18 lphaq in efficient recruitment of GRK2 to M3-ACh receptors.

19 ng on both nicotinic (nAChRs) and muscarinic ACh receptors.

20 , implying absent or otherwise dysfunctional ACh receptors.

21 processing leads to non-functional or absent ACh receptors.

22 oreactive neurons express m1-type muscarinic ACh receptors.

23 the kinetic properties of the acetylcholine (ACh) receptor.

24 nic and muscarinic classes of acetylcholine (ACh) receptors.

25 both muscarinic and nicotinic acetylcholine (ACh) receptors.

26 rneurons (ChIs) and nicotinic acetylcholine (ACh) receptors.

27 cortex (PFC) by muscarinic M1 acetylcholine (ACh) receptors.

28 rials by limiting activity of acetylcholine (ACh) receptors.

29 To determine if activation of ACh receptors account for efferent-mediated afferent exc

30 sion at 6 d after agrin removal and enhanced ACh receptor (AChR) cluster formation, but no change in

31 agrin are two opposing signals that regulate ACh receptor (AChR) clustering during neuromuscular junc

32 associated with broad bands of postsynaptic ACh receptor (AChR) clusters.

33 Centrally enriched ACh receptor (AChR) transcription and clustering were ab

34 pha subunits of the end plate acetylcholine (ACh) receptor (AChR) are described and functionally char

35 sm of inhibition of nicotinic acetylcholine (ACh) receptors (AChR) by progestin steroids.

36 cetylcholine (ACh), which binds to nicotinic ACh receptors (AChRs) on the muscle, initiating contract

37 cetylcholine (ACh) release machinery and the ACh receptors (AChRs).

38 e NMJ to bring out the function of different ACh receptors (AChRs).

39 xerts its effects exclusively through muscle ACh receptors (AChRs).

40 presses Cl(-) secretion induced by nicotinic ACh receptor activation via a Gi/o pathway.

41 lamine release were used including nicotinic ACh receptor activation, membrane depolarization with el

42 ogical results showed that alpha 7 nicotinic ACh receptor agonist infusion in the HPCd during trainin

43 lar effects were observed when the nicotinic ACh receptor agonist lobeline was used.

44 the effects of the nicotinic acetylcholine (ACh) receptor agonist dimethylphenylpiperazinium (DMPP)

45 is mapping localizes several residues of the ACh receptor alpha subunit involved in the binding of ac

46 cripts for alpha-actin, alpha-acetylcholine (ACh) receptor (alpha-AChR), desmin, muscle creatine kina

47 n of the interaction between GRK2 and the M3-ACh receptor and enhanced arrestin recruitment by these

48 u hybridization indicated the presence of m3 Ach receptor and insulin mRNA but not CCK-A or CCK-B rec

49 enerate single amino acid changes within the ACh receptor and result in prolonged channel activations

50 tes to the gating machinery of the nicotinic ACh receptor and that alphaM3 is comprised of a mixture

51 and related questions, emphasizing nicotinic ACh receptors and also discussing data from other member

52 Distinct cholinergic neurons use different ACh receptors and calcium channels in the spicule muscle

53 sker-evoked CBF responses through muscarinic ACh receptors and concurrently facilitated neuronal resp

54 nels and then focus on presynaptic nicotinic ACh receptors and presynaptic glutamate receptors.

55 The upregulation of ACh receptors and the contribution of ACh to the control

56 ulation of neuronal nicotinic acetylcholine (ACh) receptors and have recently shown that the anthelmi

57 expression in Kenyon cells and is blocked by ACh receptor antagonism.

58 of synaptic transmission and the muscarinic ACh receptor antagonist atropine.

59 In a preclinical murine model of asthma, an ACh receptor antagonist suppressed allergen-induced airw

60 The ability of the nicotinic ACh receptor antagonist vecuronium (1 microM) to depress

61 eated intranasally with different muscarinic ACh receptor antagonists and then exposed intranasally t

62 Muscarinic ACh receptor antagonists are used clinically to treat as

63 A series of clinical M3 muscarinic ACh receptor antagonists inhibited allergen-induced IL-3

64 activity was suppressed with acetylcholine (ACh) receptor antagonists and was potentiated by eserine

65 ACh receptors are established therapeutic targets for Al

66 Only functional ACh receptors are expressed on the cell surface; unassem

67 Finally, we demonstrate that nicotinic ACh receptors are localized in distinct microdomains at

68 DA](o) is lost when nicotinic acetylcholine (ACh) receptors are antagonized or when examined in stria

69 Neuronal nicotinic acetylcholine (ACh) receptors are ligand-gated, cation-selective ion ch

70 action of GRK2 with the M3-acetylcholine (M3-ACh) receptor as well as Gq-protein subunits with high s

71 alpha subunit of the Torpedo acetylcholine (ACh) receptor as well as to its V8-protease 20 kDa fragm

72 Ch, and confirm that there is no increase in ACh receptors at the junction, three characteristics dis

73 e membrane-associated Torpedo acetylcholine (ACh) receptor at 4A resolution.

74 The nicotinic acetylcholine (ACh) receptor belongs to a superfamily of synaptic ion c

75 ent and the M1-M2 loop of the acetylcholine (ACh) receptor beta subunit.

76 ment (M1) of the mouse-muscle acetylcholine (ACh) receptor beta subunit.

77 mice lacking the beta2 subunit of nicotinic ACh receptors (beta2-/-), correlated retinal waves are a

78 binding protein and the homologous nicotinic ACh receptors bind alpha-bungarotoxin at their ACh bindi

79 e that galantamine activates the muscle-type ACh receptor by interacting with a binding site that is

80 hen have a selective action at the nicotinic ACh receptor cation channel following its metabolism to

81 Mutations in muscle ACh receptors cause slow-channel syndrome (SCS) and Esco

82 Blockade of either nicotinic or muscarinic ACh receptors caused significant impairments in RAM choi

83 ACh), bind at two sites in the neuromuscular ACh receptor channel (AChR) to promote a reversible, glo

84 side chains play a relatively minor role in ACh receptor channel activation.

85 VIP, however, did not alter single ACh receptor channel current amplitude, duration of clos

86 sly probed the structure of the mouse-muscle ACh receptor channel in the resting state obtained in th

87 VIP-induced modification of nicotinic ACh receptor channel kinetics results in an increase in

88 ng sites of the neuromuscular acetylcholine (ACh) receptor channel contain several aromatic residues,

89 racetam modulation of the neuronal nicotinic ACh receptor-channel is exerted via G proteins and prote

90 84) on the neuronal nicotinic acetylcholine (ACh) receptor-channel were studied by the whole-cell pat

91 Nicotinic ACh receptor channels (AChRs) exposed to high concentrat

92 A receptors GABRA4 and GABRG1, the nicotinic ACh receptor CHRNA4 and cholinergic differentiation fact

93 Postsynaptically, ACh receptor clusters are markedly increased in number a

94 fusion, significantly larger acetylcholine (ACh) receptor clusters, and increased expression of MuSK

95 Specifically, in the absence of ACh receptors, clusters of the receptor-aggregating prot

96 The nicotinic acetylcholine (ACh) receptor converts transiently to an open-channel fo

97 The nicotinic acetylcholine (ACh) receptors cycle among classes of nonconducting rest

98 sthenia, acetylcholinesterase deficiency and ACh-receptor deficiency; but genes encoding both structu

99 raction from oriented complexes of 383C with ACh receptor-enriched membrane vesicles and electron mic

100 ely and directly suppressed alpha7-nicotinic-ACh receptor-expressing interstitial, but not alveolar,

101 However, if nicotine activated ACh receptors found in muscle as potently as it does bra

102 newly described effect of phosphorylation on ACh receptor function may serve as an important modulato

103 by [(125)I]-alpha-bungarotoxin binding, and ACh receptor function was evaluated by using a two-elect

104 cell (LC), uses an M1/M3/M5-like muscarinic ACh receptor GAR-3 to receive extrasynaptic ACh signalin

105 The activation of muscarinic ACh receptors generated a biphasic modulation of synapti

106 lectron microscopic study of the muscle-type ACh receptor had suggested that a local disturbance in t

107 on of nicotine on brain compared with muscle ACh receptors has not been determined.

108 The neuromuscular acetylcholine (ACh) receptor has two conserved prolines in loop D of th

109 These results indicate that NAc ACh receptors have opposing roles in maintaining learned

110 KEY POINTS: Neuromuscular acetylcholine (ACh) receptors have a high affinity for the neurotransmi

111 Neuromuscular acetylcholine (ACh) receptors have a high affinity for the neurotransmi

112 Torpedo electroplax nicotinic acetylcholine (ACh) receptors have shown that entry into the desensitiz

113 ffect was phenocopied by knockdown of the M1 ACh receptor in V1, indicating that this modulation of i

114 r autocrine action through the M3 muscarinic ACh receptors in HBE cells suppressed allergen-induced A

115 ence study of the membrane redistribution of ACh receptors in keratinocytes exposed to a DC field rev

116 The results suggest that muscarinic ACh receptors in the caudomedial NAcc may play a role in

117 Here, we demonstrate a role for NAc ACh receptors in the flexibility of sign-tracking.

118 confirmed that both nicotinic and muscarinic ACh receptors in the ventral hippocampus play a signific

119 neuregulin (NRG) on nicotinic acetylcholine (ACh) receptors in interneurons located in the stratum ra

120 The acetylcholine (ACh) receptors in muscle have the composition alpha2beta

121 finity binding of nicotine to acetylcholine (ACh) receptors in the brain.

122 ate the lLN(v)s possess excitatory nicotinic ACh receptors, inhibitory ionotropic GABA(A) receptors,

123 nces the extent and stability of the GRK2-M3-ACh receptor interaction, and that not only Gbetagamma b

124 e, which is similar to that of the nicotinic ACh receptor, involves a vapor-lock mechanism where limi

125 low affinity for nicotine at the muscle-type ACh receptor is largely due to the fact that this key in

126 Direct synaptic modulation mediated by ACh receptors is only evident at the A/C synapse, where

127 apable of self-aggregation, interaction with ACh receptors is required for proper subsynaptic localiz

128 Assembly of ACh receptors is under tight quality control.

129 The nicotinic acetylcholine (ACh) receptor is a neurotransmitter-gated ion channel co

130 ting channel of the nicotinic acetylcholine (ACh) receptor is lined by the first (M1) and second (M2)

131 The nicotinic acetylcholine (ACh) receptor is the neurotransmitter-gated ion channel

132 to involve defects in the functioning of the ACh receptor itself.

133 out an increase in the area and intensity of ACh receptor labeling at the neuromuscular junction (NMJ

134 surface receptors referred to as muscarinic ACh receptors (M(1)-M(5) mAChRs).

135 the five mammalian muscarinic acetylcholine (ACh) receptors, M(5) is the only subtype expressed in mi

136 irenzepine-sensitive, Gq-coupled) muscarinic ACh receptor (m1AChR).

137 lls expressing the muscarinic acetylcholine (ACh) receptor M3 were used as ACh biosensors to record A

138 meric epitope segments (ES) of M3 muscarinic ACh receptor (M3AR) targeted by different anti-M3AR AuAb

139 uAb against the M3 muscarinic acetylcholine (ACh) receptor (M3AR) that plays an important role in reg

140 While the muscarinic ACh-receptors M3R and M1R are activating, M2R is inhibit

141 le of mAChRs, particularly the M3 muscarinic ACh receptor (M3R), in regulating the cytokine and chemo

142 as shown that M(3) muscarinic acetylcholine (ACh) receptors (M3Rs) expressed by pancreatic beta cells

143 ic glutamate receptor (mGluR) and muscarinic Ach receptor (mAchR) activation can cause rhythmic burst

144 Prolonged ("tonic") muscarinic ACh receptor (mAChR) activation increases the excitabili

145 dicating that it requires ACh and muscarinic ACh receptor (mAChR) activation.

146 iated depolarizing potentials and muscarinic ACh receptor (mAChR)-mediated hyperpolarizing potentials

147 endogenous ACh to both nAChR and muscarinic ACh receptors (mAChR) stimulate growth of both small cel

148 terest in the M(1) muscarinic acetylcholine (ACh) receptor (mAChR) has led to the discovery of variou

149 rs (nAChRs) and G protein-coupled muscarinic ACh receptors (mAChRs) are expressed on rat hippocampal

150 show that stimulation of m1 or m3 muscarinic ACh receptors (mAChRs) for 2min potentiates recombinant

151 d inhibition via activation of muscarinic m2 ACh receptors (mAChRs) linked to inward rectifier potass

152 ver, it remains controversial how muscarinic ACh receptors (mAChRs) modulate striatal DA release, wit

153 acetylcholine (ACh) and activates muscarinic ACh receptors (mAChRs) post-synaptically on airway smoot

154 s in levels of the M1, M2, and M4 muscarinic ACh receptors (mAChRs), but no alterations in dopamine r

155 nic ACh receptors (nAChRs) and M2 muscarinic ACh receptors (mAChRs), respectively.

156 athetic actions via activation of muscarinic ACh receptors (mAChRs), we examined the potential metabo

157 em, modulates immune function via muscarinic ACh receptors (mAChRs).

158 Muscarinic and nicotinic acetylcholine (ACh) receptors (mAChRs and nAChRs) are emerging as impor

159 q -coupled M1-type muscarinic acetylcholine (ACh) receptors (mAChRs) mediate two distinct electrophys

160 q -coupled M1-type muscarinic acetylcholine (ACh) receptors (mAChRs) mediate two distinct electrophys

161 modulator of M(4) muscarinic acetylcholine (ACh) receptors (mAChRs) on the basis of its ability to p

162 combined with muscarinic (m) acetylcholine (ACh) receptors (mAChRs) with immunocytochemistry to iden

163 Forebrain muscarinic acetylcholine (ACh) receptors (mAChRs; M1-M5) are predicted to play imp

164 gh allosterically activated alpha7 nicotinic ACh receptor may affect intracellular calcium levels, su

165 The stimulation of the ACh receptor may be directly related to the cognitive en

166 amate secretion via nicotinic and muscarinic ACh receptor-mediated pathways, respectively.

167 st be taken into consideration in studies of ACh receptor-mediated synaptic efficacy in the CNS.

168 At the neuromuscular junction, the nicotinic ACh receptor mediates postsynaptic depolarization, and a

169 ratinocyte desmogleins (Dsg), acetylcholine (ACh) receptors, mitochondrial proteins, and some other s

170 ligand binding in other AChBPs and nicotinic ACh receptor (nAChR) alpha subunits.

171 This increase is blocked by a nicotinic ACh receptor (nAChR) antagonist.

172 -D-aspartate receptor (NMDAR)] and nicotinic ACh receptor (nAChR) antagonists.

173 alpha4 and alpha7 subunits of the nicotinic ACh receptor (nAChR) before and after coitus was determi

174 in the alpha subunit of the muscle nicotinic ACh receptor (nAChR) expressed in Xenopus oocytes.

175 mRNA levels of alpha9 and alpha10 nicotinic ACh receptor (nAChR) genes.

176 To determine the predominant nicotinic ACh receptor (nAChR) located on neurones in the dorsal m

177 The a7 nicotinic ACh receptor (nAChR) subtype is highly expressed through

178 The alpha7 nicotinic ACh receptor (nAChR) subtype is highly expressed through

179 ls of fluorescent alpha4 and beta2 nicotinic ACh receptor (nAChR) subunits.

180 lices, we found that ACh generated nicotinic ACh receptor (nAChR)-mediated depolarizing potentials an

181 ucidate this mechanism by studying nicotinic ACh receptor (nAChR)-mediated responses.

182 cific deficits in beta2-containing nicotinic ACh receptor (nAChR)-modulation of electrically evoked d

183 steric potentiating effects at the nicotinic ACh receptor (nAChR).

184 Nicotinic acetylcholine (ACh) receptor (nAChR) agonists are potential therapeutic

185 The nicotinic acetylcholine (ACh) receptor (nAChR) is the principal insecticide targe

186 The nicotinic acetylcholine (ACh) receptor (nAChR) plays a crucial role in excitatory

187 tions at the muscle nicotinic acetylcholine (ACh) receptor (nAChR), a rhodamine fluorophore was tethe

188 ogenous nicotine to nicotinic acetylcholine (ACh) receptors (nAChR) and the binding of endogenous ACh

189 n between ACh and DA signaling via nicotinic ACh receptors (nAChRs) and DA D2 receptors (D2Rs).

190 tylcholine (ACh) signaling through nicotinic ACh receptors (nAChRs) and downstream T-type voltage-dep

191 Cys-loop ligand-gated nicotinic ACh receptors (nAChRs) and G protein-coupled muscarinic

192 vation of postsynaptic alpha4beta2 nicotinic ACh receptors (nAChRs) and M2 muscarinic ACh receptors (

193 nergistically via their actions at nicotinic ACh receptors (nAChRs) and NMDA receptors, respectively.

194 Alpha6-containing (alpha6*) nicotinic ACh receptors (nAChRs) are selectively expressed in dopa

195 d function of presynaptic neuronal nicotinic ACh receptors (nAChRs) at the major inputs to MGB and ch

196 1)(2)(5)I]-bungarotoxin binding to nicotinic ACh receptors (nAChRs) containing beta2 or alpha7 subuni

197 Activation of presynaptic nicotinic ACh receptors (nAChRs) enhances GABAergic transmission.

198 Nicotinic ACh receptors (nAChRs) have been implicated in a variety

199 eceptors (NMDARs), neuronal alpha7 nicotinic ACh receptors (nAChRs) have been implicated in neuronal

200 udy we characterized properties of nicotinic ACh receptors (nAChRs) in cultured cat glomus cells usin

201 actory bulb to examine the role of nicotinic ACh receptors (nAChRs) in regulating the responses of mi

202 ction and pharmacology of neuronal nicotinic ACh receptors (nAChRs) in young adult and the aged rat M

203 neuromuscular junction, cycling of nicotinic ACh receptors (nAChRs) is critical for the maintenance o

204 l DA release through activation of nicotinic ACh receptors (nAChRs) on DA axonal projections.

205 ns, striatal cholinergic tone, and nicotinic ACh receptors (nAChRs) on DA presynaptic terminals.

206 gle channel properties of neuronal nicotinic ACh receptors (nAChRs) were investigated in outside-out

207 Neuronal nicotinic ACh receptors (nAChRs) were studied in the rat hippocamp

208 ro-beta-erythroidine (DHbetaE) for nicotinic ACh receptors (nAChRs), 2 mM kynurenate (Kyn) for glutam

209 oline (ACh)-gated ion channels, or nicotinic ACh receptors (nAChRs), mediate the nicotinergic signali

210 nvolve stimulation of alpha4beta2* nicotinic ACh receptors (nAChRs), systemic administration of the p

211 the alpha4 subunit of the neuronal nicotinic ACh receptors (nAChRs), the latter of which has been sho

212 ) acts in part through a family of nicotinic ACh receptors (nAChRs), which mediate diverse physiologi

213 g RGCs through alpha-Bgt-sensitive nicotinic ACh receptors (nAChRs).

214 e, consistent with the presence of nicotinic ACh receptors (nAChRs).

215 zes calyceal endings by activating nicotinic ACh receptors (nAChRs).

216 ylcholine (ACh) activates calyceal nicotinic ACh receptors (nAChRs); however, it is unclear whether t

217 containing alpha3 subunits [alpha3-nicotinic ACh receptors (nAChRs)] and those containing alpha7 subu

218 romeric alpha3beta4 nicotinic acetylcholine (ACh) receptors (nAChRs) are pentameric ligand-gated cati

219 rotective agent and nicotinic acetylcholine (ACh) receptors (nAChRs) as targets for neuroprotection,

220 odulators (PAMs) of nicotinic acetylcholine (ACh) receptors (nAChRs) have potential clinical applicat

221 ) and activation of nicotinic acetylcholine (ACh) receptors (nAChRs) in DA neuron (DAN) axons.

222 esent study, these ionotropic acetylcholine (ACh) receptors (nAChRs) were activated by levamisole and

223 o activation of the nicotinic acetylcholine (ACh) receptors (nAChRs), mainly alpha7 nAChR, expressed

224 to inhibit neuronal nicotinic acetylcholine (ACh) receptors (nnAChRs) expressed in Xenopus laevis ooc

225 dings suggest that alpha9 contributes to the ACh receptor of avian hair cells and supports the genera

226 The acetylcholine (ACh) receptor of the hair cell is a ligand-gated cation

227 Through the expression of m1 ACh receptors on nearly all of these PV cells, the choli

228 with the existence of facilitatory nicotinic ACh receptors on the motor nerve endings.

229 acing positions of the muscle acetylcholine (ACh) receptor (one position at a time), including the po

230 that galantamine can activate the nicotinic ACh receptor or modulate its activation by ACh.

231 directly activate the muscle-type nicotinic ACh receptor or to modulate receptor activation by selec

232 conserved circuit, activation of muscarinic ACh receptors revealed marked differences in cholinergic

233 Nicotinic acetylcholine (ACh) receptor-rich patches prepared from rat myotubes we

234 otion: MscL tilts its helices, the nicotinic ACh receptor rotates its helices, and KirBac1.1 bends it

235 injection of either alpha7-nAChR (nicotinic ACh receptor)-selective [methyllycaconitine (MLA)] or be

236 found in muscle as potently as it does brain ACh receptors, smoking would cause intolerable and perha

237 M3-ACh receptor stimulation with 10 microM acetylcholine re

238 r homology model based on the acetylcholine (ACh) receptor structure is complicated by the low sequen

239 gonist at the M(2) muscarinic acetylcholine (ACh) receptor subtype that was designed using a multival

240 ulated by distinct muscarinic acetylcholine (ACh) receptor subtypes, we inactivated signaling through

241 Furthermore, reducing nicotinic ACh receptor subunit expression in MBONs compromises odo

242 using mutants lacking a functional nicotinic ACh receptor subunit or through muscle-specific expressi

243 tified a novel motif in the M1 domain of the ACh-receptor subunit that is responsible for ER retentio

244 wo alternative extended conformations of the ACh receptor subunits, one characteristic of either alph

245 ting from mutations in muscle acetylcholine (ACh) receptor subunits.

246 e inhibitors of the nicotinic acetylcholine (ACh) receptors suppress cation flux directly by binding

247 In sympathetic neurons, muscarinic M1 ACh receptor suppression of the Ca2+ current (ICa) was t

248 dulation depend on the subtype of muscarinic ACh receptors that are activated.

249 ogical, functional and structural studies of ACh receptors, the basis for the differential action of

250 In adult-type ACh receptors, the energy from the affinity change for A

251 regulate metabolic processes; (ii) form new ACh receptors via ACh mRNA activity; (iii) mediate atten

252 ral cortex contains nicotinic acetylcholine (ACh) receptors vital to cortical function.

253 ization was still observed if the muscarinic ACh receptor was bypassed and the channel was activated

254 inacrine in the open channel of mouse-muscle ACh receptor was mapped in cysteine-substituted mutants

255 sidues on the three-dimensional model of the ACh receptor, we have employed a combination of X-ray di

256 horylation on desensitization of muscle-type ACh receptors, we expressed the frog embryonic receptor

257 g of acetylcholine (ACh) by the mouse muscle ACh receptor, were each mutated to nine other residues,

258 mitter ACh but utilize distinct postsynaptic ACh receptors, whose distinct biophysical properties con

259 omparison of the extracellular domain of the ACh receptor with an ACh-binding protein (AChBP) to whic

260 Treatment of embryonic muscle ACh receptors with 8-Br cAMP had no measurable effect on