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 only used to immunolocalize alpha7 nicotinic ACh receptors.

9 o the extracellular domains of the nicotinic ACh receptors.

10 reveal the basis for agonist recognition by ACh receptors.

11 ebrafish to mutant fish lacking postsynaptic ACh receptors.

12 regulating surface trafficking of functional ACh receptors.

13 cle that involves activation of postsynaptic ACh receptors.

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

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

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

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

18 , implying absent or otherwise dysfunctional ACh receptors.

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

20 oreactive neurons express m1-type muscarinic ACh receptors.

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

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

23 both muscarinic and nicotinic acetylcholine (ACh) receptors.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

55 ACh receptors are established therapeutic targets for Al

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

111 Assembly of ACh receptors is under tight quality control.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

163 1)(2)(5)I]-bungarotoxin binding to nicotinic ACh receptors (nAChRs) containing beta2 or alpha7 subuni

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

202 M3-ACh receptor stimulation with 10 microM acetylcholine re

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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