ライフサイエンスコーパス: muscarinic receptor

1 HT(2A)) or scopolamine (an antagonist of the muscarinic receptor).

2 ta2-adrenergic receptor (beta2AR) and the M2 muscarinic receptor.

3 not exhibit SOCE following activation of the muscarinic receptor.

4 he quaternary organization of the related M3 muscarinic receptor.

5 t some neurons in nP, TS, and tectum express muscarinic receptors.

6 ing cholinergic system through nicotinic and muscarinic receptors.

7 This effect was mainly mediated by muscarinic receptors.

8 Solely by Synthetic Ligand (RASSL) forms of muscarinic receptors.

9 were mediated by co-activation of M1 and M3 muscarinic receptors.

10 CNQ channels and is known to be inhibited by muscarinic receptors.

11 acetylcholine, the latter occurring through muscarinic receptors.

12 e from mossy fibers by acting on presynaptic muscarinic receptors.

13 eric activation and allosteric modulation of muscarinic receptors.

14 ation mechanism and allosteric modulation of muscarinic receptors.

15 sure of the agonist to a wider population of muscarinic receptors.

16 cells, which express the beta-adrenergic and muscarinic receptors.

17 t involves direct antagonism of M1 and/or M3 muscarinic receptors.

18 d RGS4, a negative regulator of beta-cell M3 muscarinic receptors.

19 edominantly by parasympathetic activation of muscarinic receptors.

20 pharmacological inhibition of purinergic and muscarinic receptors.

21 t evoked by activation of expressed m1 or m3 muscarinic receptors.

22 d acetylcholine release via activation of M1 muscarinic receptors.

23 tivity on signal transduction via Gq-coupled muscarinic receptors.

24 neurons through presynaptic and postsynaptic muscarinic receptors.

25 uately explained solely by its antagonism at muscarinic receptors.

26 parasympathetic ACh slows the heart through muscarinic receptors.

27 ions (basket cells, BCs) were depolarized by muscarinic receptors.

28 that this effect is mediated exclusively by muscarinic receptors.

29 neurotransmitter acetylcholine, we show that muscarinic receptors 1 and 3 (m1 and m3) are highly expr

30 al proliferation and tumorigenesis in an ACh muscarinic receptor-3 (M3R)-dependent manner, in part th

31 l subunits [Cacna1c and Cacnb2], cholinergic muscarinic receptor 4 [Chrm4)], dopamine receptor D2 [Dr

32 The X-ray crystal structure of the M2 muscarinic receptor, a key GPCR that regulates human hea

33 beta1AR) and activating autoantibodies to M2 muscarinic receptors (AAM2R) in the genesis of atrial fi

34 ium channels is sufficient to reconstitute a muscarinic receptor-activated inward aftercurrent in hum

35 tro by pairing white matter stimulation with muscarinic receptor activation at a fixed interval and s

36 We tested whether M1 muscarinic receptor activation enhances glutamatergic sy

37 Muscarinic receptor activation facilitates the induction

38 Insulin secretion was shown to be induced by muscarinic receptor activation in a pancreatic beta cell

39 Muscarinic receptor activation in these cells appears to

40 receptor type contributions, we find that m2 muscarinic receptor activation increases glomerular sens

41 In contrast, muscarinic receptor activation increases mitral cell spi

42 Previous studies have suggested that muscarinic receptor activation modulates glutamatergic t

43 Muscarinic receptor activation resulting from ACh releas

44 d from lacrimal glands, we demonstrated that muscarinic receptor activation stimulates a phospholipas

45 omponents of the signalling pathway coupling muscarinic receptor activation to changes in chemorecept

46 Moreover, muscarinic receptor activation, and in particular M2 sub

47 Although PV BCs were also excited by muscarinic receptor activation, they more frequently res

48 obust and more sustained increase induced by muscarinic receptor activation.

49 trinsic glial properties related to enhanced muscarinic receptor activation.

50 ter the stimulation paradigm and were due to muscarinic receptor activation.

51 nt in Tg.sgk-SCG neurons was counteracted by muscarinic receptor activation.

52 ayed increase in excitability in response to muscarinic receptor activation.

53 y TRPV1 activation but not that evoked by M1 muscarinic receptor activation.

54 d theta oscillations, and both nicotinic and muscarinic receptor activity contributed to this process

55 The muscarinic receptor agonist 'BuTAC' was previously shown

56 RTN chemoreceptors to ACh was mimicked by a muscarinic receptor agonist (oxotremorine; 1 mum), and b

57 The muscarinic receptor agonist carbachol activated ERK1/2 b

58 orylation of Ser-2808 in RyR2 induced by the muscarinic receptor agonist carbachol is mediated by a s

59 ncreased as rapidly as that initiated by the muscarinic receptor agonist carbachol, which promoted an

60 Effects of a muscarinic receptor agonist oxotremorine-M (oxo-M) on bl

61 that SPARC enhanced the promoting effect of Muscarinic receptor agonist oxotremorine-M on insulin se

62 Carbachol, a known nAChR and muscarinic receptor agonist, up-regulated both alpha4bet

63 uction following injection of pilocarpine, a muscarinic receptor agonist.

64 served more than 30 min after removal of the muscarinic receptor agonist.

65 ationship between the efficacy of seven M(3) muscarinic receptor agonists and their rate of dissociat

66 Muscarinic receptor agonists are characterized by appare

67 currently limited to medications (e.g., the muscarinic receptor agonists pilocarpine and cevimeline)

68 salivation are limited to medications (e.g., muscarinic receptor agonists: pilocarpine and cevimeline

69 20 to probe specifically the human M2 and M4 muscarinic receptor allosteric binding sites.

70 scarinic receptors, and stimulation of these muscarinic receptors also correlated with a 2-fold incre

71 GABAA-LTP requires the activation of M1-muscarinic receptors and an increase in cytosolic Ca(2+)

72 Moreover, at least in the airways, muscarinic receptors and beta-adrenoceptors are expresse

73 Muscarinic receptors and beta-adrenoceptors are physiolo

74 suggested that lipid rafts colocalized both muscarinic receptors and channel subunits to enable rece

75 hat this population expressed adrenergic and muscarinic receptors and displayed transcriptional profi

76 to the efficient coupling between endogenous muscarinic receptors and GIRK channels, we found that fi

77 These effects are mediated by M1-type muscarinic receptors and occur in a casein kinase-2-depe

78 -regulated lung expression of M1, M2, and M3 muscarinic receptors and phosphodiesterase (PDE)4D5 isoz

79 garding the intrinsic voltage sensitivity of muscarinic receptors and the consequences of this intrig

80 nges, which involved the mechanisms of BDNF, muscarinic receptors, and beta3-adrenoceptor expression.

81 tor rolipram attenuates the increase in AHR, muscarinic receptors, and PDE4D5, but fails to down-regu

82 ologically to involve endogenously expressed muscarinic receptors, and stimulation of these muscarini

83 Here we show that muscarinic receptor antagonism at the hypoglossal motor

84 Here, we find that nonselective muscarinic receptor antagonism in mice as well as epithe

85 In addition, a muscarinic receptor antagonist reduces LID.

86 formance was facilitated by the nonselective muscarinic receptor antagonist scopolamine as well as th

87 ction would improve depressive symptoms, the muscarinic receptor antagonist scopolamine manifested an

88 ing iontophoretic application of the general muscarinic receptor antagonist scopolamine with single-c

89 This study tests the hypothesis that muscarinic receptor antagonist therapy with tiotropium b

90 studies have suggested that the long-acting muscarinic receptor antagonist tiotropium, a drug widely

91 ent and the ratio of those using long-acting muscarinic receptor antagonist were higher than those in

92 gonist), or methoctramine (a selective M2/M4 muscarinic receptor antagonist).

93 Here, we show that the muscarinic receptor antagonist, atropine, eliminated the

94 treatment with solifenacin, an FDA-approved muscarinic receptor antagonist, increased oligodendrocyt

95 0, 0.03, or 0.1 mg/kg, intraperitoneally), a muscarinic receptor antagonist, or mecamylamine (0, 0.75

96 es report that scopolamine, an acetylcholine muscarinic receptor antagonist, produces rapid antidepre

97 herapy with tiotropium bromide, an M1 and M3 muscarinic receptor antagonist, will decrease the airway

98 either saline or scopolamine, a nonselective muscarinic receptor antagonist.

99 of scopolamine, a nonselective acetylcholine muscarinic receptor antagonist.

100 haled bronchodilators, including long-acting muscarinic receptor antagonists (LAMA) and long-acting b

101 Muscarinic receptor antagonists and beta-adrenoceptor ag

102 ntribute to a rationale for a combination of muscarinic receptor antagonists and beta-adrenoceptor ag

103 of long-acting beta(2) agonists/long-acting muscarinic receptor antagonists as the preferred treatme

104 Nicotinic but not muscarinic receptor antagonists block allergen- or nicot

105 nd can be reliably and completely blocked by muscarinic receptor antagonists.

106 rendered ineffective by either nicotinic or muscarinic receptor antagonists.

107 my, 4) nicotinic receptor (mecamylamine) and muscarinic receptor (AQ-RA 741) blockade, and 5) ex vivo

108 c activation is less well understood, though muscarinic receptors are implicated in olfactory learnin

109 Our study identified muscarinic receptor as a key target of i-Extract, provid

110 3), we used carbachol, a ligand specific for muscarinic receptor, as the secretagogue.

111 usly shown that dendritic cells (DC) express muscarinic receptors, as well as the enzymes responsible

112 To assess the role played by the muscarinic receptors at the hippocampal-frontal cortex s

113 t study, by expressing an arrestin-biased M3 muscarinic receptor-based DREADD (M3D-arr) in stable hER

114 tudy, we describe the development of an M(3) muscarinic receptor-based DREADD [Rq(R165L)] that is no

115 orylation site in a region homologous to the muscarinic receptor-binding site of Tau suggests that MA

116 Here, we examined the effects of muscarinic receptor blockade on rule-related activity in

117 Overall, our results suggest that muscarinic receptor blockade results in a bona fide lear

118 iated since they were eliminated by systemic muscarinic receptor blockade.

119 -like behavior and which are reversed by the muscarinic receptor blockade.

120 port the crystal structures of the M1 and M4 muscarinic receptors bound to the inverse agonist, tiotr

121 Transient activation of muscarinic receptors by carbachol results in a long-last

122 Recently, we found that bivalent agonists of muscarinic receptors can simultaneously occupy both the

123 (MDD) in or close to a region containing the muscarinic receptor CHRM2 gene.

124 lycemia was abolished by blocking peripheral muscarinic receptors, consistent with the hypothesis tha

125 ACh, via M2 muscarinic receptors, contributes to the modulation and

126 e et al. (2017) demonstrate that presynaptic muscarinic receptors counteract the effects of dopamine

127 um and exhibited 19-fold selectivity against muscarinic receptor-coupled TRPC6 channel activation.

128 xperiments, whereas blockade of nicotinic or muscarinic receptors decreased perceptual discrimination

129 bdivision; 3) distinct kainate, alpha2 , and muscarinic receptor densities that rendered distinctive

130 disease brain usurp endogenous acetylcholine muscarinic receptor-dependent long-term depression, to e

131 elial cell adhesion molecule expression in a muscarinic receptor-dependent manner.

132 odulate the SCA-induced locomotor rhythm via muscarinic receptor-dependent mechanisms and that the mo

133 r cholinergic constraint that is mediated by muscarinic receptor-dependent regulation of mitochondria

134 1) quinone reductase 2 (QR2) expression is a muscarinic-receptor-dependent removable constraint on me

135 Blocking muscarinic receptors depressed taste-evoked responses in

136 Block of muscarinic receptors did not affect action potentials or

137 We found that stimulation of muscarinic receptors, either by an agonist or by the syn

138 Muscarinic receptors endogenous to HEK293 cells were ide

139 f these agents depends on the blockade of M3 muscarinic receptors expressed on airway smooth muscle c

140 40 diminished eNOS and nNOS as well as M1-M4 muscarinic receptor expression and also affected puriner

141 eased AHR might reflect increased PDE4D5 and muscarinic receptor expression, the mechanisms underlyin

142 These results suggest that activation of muscarinic receptors facilitates mechano-sensitive, caps

143 Each subtype of the muscarinic receptor family of G protein-coupled receptor

144 orthosteric ligand, acetylcholine, at the M1 muscarinic receptors found in higher concentrations in t

145 The alteration of PSC muscarinic receptor functions also persists during the p

146 The procedure was verified at M(2) and M(4) muscarinic receptors fused with the G(15) G-protein alph

147 modulation of signals transduced by the M(3) muscarinic receptor/G(q)/PLCbeta pathway at the plasma m

148 and chrm5b, isolated here, as well as other muscarinic receptor genes and their duplicates and sugge

149 Blockade of muscarinic receptors had no effect on evoked dopamine re

150 Nicotinic and muscarinic receptors have been found on both the sensory

151 Although muscarinic receptors have been implicated in executive p

152 lidal MSN activity via a Gq-coupled human M3 muscarinic receptor (hM3Dq), a type of designer receptor

153 Using the activatory Gq-coupled human M3 muscarinic receptor (hM3Dq), we found that chemogenetic

154 Antagonizing the human M3 muscarinic receptor (hM3R) over a long time is a key fea

155 ocus, using viral expression of the modified muscarinic receptor hM4Di.

156 Cholinergic drugs acting at M1/M4 muscarinic receptors hold promise for the treatment of s

157 Activation of these endogenous muscarinic receptors however, failed to suppress express

158 Blocking muscarinic receptors impairs learning for nearly all odo

159 muscarinic acetylcholine receptor, the major muscarinic receptor in beta cells.

160 79 or AKAP15, rescued suppression of I(M) by muscarinic receptors in AKAP150(-/-) neurons.

161 lexander disease patients, and that blocking muscarinic receptors in Alexander disease model mice red

162 tter ACh targets nicotinic (nAChRs), but not muscarinic receptors in bone cells, affecting mainly ost

163 These results demonstrate that blockade of muscarinic receptors in DLPFC creates deficits in workin

164 The finding that blockade of muscarinic receptors in mPFC impaired trace conditioning

165 synaptic activity mediated by M(1) and M(2) muscarinic receptors in MSNs, consisting of an increase

166 x behavior of oligomers is characteristic of muscarinic receptors in myocardial preparations.

167 del suggests that the roles of nicotinic and muscarinic receptors in olfactory bulb are both distinct

168 ts encourage a more general understanding of muscarinic receptors in PR and they motivate additional

169 ed M2 muscarinic receptor were compared with muscarinic receptors in sarcolemmal membranes for the ef

170 These results indicate that muscarinic receptors in striatal output neurons reliably

171 direct activation of G protein-coupled, M(3) muscarinic receptors in the absence of exogenous agonist

172 ral blockade of cholinergic nicotinic and/or muscarinic receptors in the OB.

173 output under control conditions but not when muscarinic receptors in the RTN are blocked.

174 The present study evaluated the role of PR muscarinic receptors in trace fear conditioning.

175 chol was blocked by antagonists of M1 and M3 muscarinic receptors in two subpopulations of BF GABAerg

176 We also evaluate the ability of muscarinic receptors, in particular the M2 subtype, to m

177 , previous work suggested a role of ACh, via muscarinic receptors, in the modulation of information t

178 from their striatal terminals, activation of muscarinic receptors induced Ca2+ mobilization and inwar

179 estigated the molecular basis underlying the muscarinic receptor-induced afterdepolarization using mo

180 RPC5 or TRPC6 enhances, the amplitude of the muscarinic receptor-induced inward aftercurrent.

181 ults indicate that TRPC channels mediate the muscarinic receptor-induced slow afterdepolarization see

182 ically encoded biosensor, that activation of muscarinic receptor induces the breakdown of phosphatidy

183 nt of cells expressing such mutants with the muscarinic receptor inverse agonist atropine increased c

184 The M2 muscarinic receptor is the prototypic model of allostery

185 Acetylcholine (ACh) modulation, through muscarinic receptors, is a particularly widespread mecha

186 which is a known allosteric modulator of the muscarinic receptors, is also shown to be a modulator of

187 For the M(2) muscarinic receptor, it was further shown that depolariz

188 Q K(+) channel current by activation of M(1) muscarinic receptors; KCNQ channels require PIP(2) for t

189 tussis toxin or in myocytes from M2- or M1/3-muscarinic receptor knockout mice, atropine increased cA

190 or genetic disruption of the stromal type 1 muscarinic receptor, leading to improved survival of the

191 ein kinase C-dependent event promoted by the muscarinic receptor ligand carbachol in freshly disperse

192 to bind acetylcholine (ACh), the endogenous muscarinic receptor ligand, but can be efficiently activ

193 )-coupled DOR and the Galpha(q)-coupled M(3) muscarinic receptor (M(3)R) was increased but not signal

194 enzyme-linked immunosorbent assay for all 5 muscarinic receptors (M(1) -M(5) ), we identified in the

195 Chronic stimulation of M(2) muscarinic receptors (M(2)Rs) causes internalization of

196 and Galpha(1)(3) coupled receptors (such as muscarinic receptor, m1, and thrombin receptor, PAR-1) a

197 ct the PM localization or function of the M1 muscarinic receptor (M1R)/Gq signaling cascade.

198 orded with another cognate G protein-coupled muscarinic receptor, M1R.

199 ized the oligomeric status of eGFP-tagged M2 muscarinic receptor (M2R) and Gi1 by single-particle pho

200 -2 regulates expression of the C. elegans M2 muscarinic receptor (m2R) ortholog, GAR-2.

201 eta-arrestin 1 (betaarr1) in complex with M2 muscarinic receptor (M2R) reconstituted in lipid nanodis

202 tic regulation of HR and the prototypical M2 muscarinic receptor (M2R)-dependent signaling pathway in

203 eceptor that activates KACh channels, the M2 muscarinic receptor (M2R).

204 Activation of M2 muscarinic receptors (M2Rs) in the rat anterior basolate

205 Based on our expertise with type 3 muscarinic receptor (M3), we used carbachol, a ligand sp

206 with the third intracellular loop of the M3 muscarinic receptor (M3-MR), and SET knockdown with smal

207 evidence for a direct interaction between M3 muscarinic receptor (M3R) and PLCbeta3.

208 esonance energy transfer studies with the M3 muscarinic receptor (M3R), a prototypic class A GPCR, th

209 beta-Cell M3 muscarinic receptors (M3Rs) are known to play an essenti

210 monstrated that activation of beta-cell M(3) muscarinic receptors (M3Rs) greatly promotes glucose-sti

211 endogenous cholinergic signaling through M4 muscarinic receptors (M4Rs) promoted long-term depressio

212 In this study, we determined which muscarinic receptor (mAChR) subtypes are present in the

213 We partially cloned three subtypes of muscarinic receptors (mAChR2, -3, and -4) from brain tis

214 Indeed, muscarinic receptors (mAChRs) regulate the repair phenot

215 odulates glutamate release via activation of muscarinic receptors (mAchRs), although the consequences

216 tylcholine receptors, nicotinic (nAChRs) and muscarinic receptors (mAChRs), are expressed by vestibul

217 adoxical excitation was caused by overactive muscarinic receptors (mAChRs), leading to a switch in D2

218 We propose that the M3 muscarinic receptor maximizes the efficiency of PLCbeta3

219 Both receptors mediate Ca2+ influx whereas muscarinic receptors may also recruit Ca2+-sensitization

220 duplicates and suggests previously described muscarinic receptors may need to be reclassified.

221 ayers of primary motor cortex (M1) through a muscarinic-receptor mediated mechanism, gamma oscillatio

222 This occurs in part via transient-evoked muscarinic receptor-mediated high-frequency oscillations

223 A similar loss of muscarinic receptor-mediated suppression of M current na

224 h excited c-ACs, but inhibited NGFCs through muscarinic receptor-mediated, IP3 receptor-dependent ele

225 The G-protein-coupled muscarinic receptor mimetic carbachol, the phorbol ester

226 This interaction was specific with regard to muscarinic receptor (MR) and AGAP subtypes, and mediated

227 beta(2)-adrenergic and M(2)-muscarinic receptor mRNA and beta(2)-receptor protein we

228 Sites labeled for the three muscarinic receptor mRNAs were found in various brain re

229 electivity, has been increasingly applied to muscarinic receptors (MRs).

230 ergic tone or antagonizing postsynaptic M(1) muscarinic receptors normalized synaptic activity.

231 Activation of M1 muscarinic receptors occurs through orthosteric and allo

232 (ACh) from medial septal afferents activates muscarinic receptors on both vasoactive intestinal pepti

233 g through the thalamic radiation activate M1 muscarinic receptors on TC projections and sustain gluta

234 arasympathetic nerves blocks inhibitory M(2) muscarinic receptors on the parasympathetic nerves, incr

235 e-dependent inhibition of DA release through muscarinic receptors only in the shell, where higher act

236 uire inhibitory action of either presynaptic muscarinic receptors or presynaptic cannabinoid receptor

237 l, inhibiting the effects of ACh by blocking muscarinic receptors, or by selectively activating hyper

238 ACh accessibility to a select population of muscarinic receptors, possibly only those expressed by I

239 be partially attributed to the M2 subtype of muscarinic receptors, possibly through a combination of

240 cal blockade of nicotinic receptors, but not muscarinic receptors, prevented heart block and mortalit

241 Stimulation of muscarinic receptors promotes memory consolidation in se

242 We performed muscarinic receptor radioligand binding.

243 r, the majority of the VF neurons express M2 muscarinic receptors, raising the possibility that the e

244 Activation of muscarinic receptors recruits CPI-17, but not MYPT1-medi

245 Muscarinic receptors regulate airway smooth muscle tone,

246 M1 muscarinic receptors regulate the phosphorylation of AMP

247 , Shen et al. (2015) demonstrate that the M4 muscarinic receptor regulates striatal plasticity.

248 Muscarinic receptors represent a promising therapeutic t

249 tylcholine (ACh) that bind to purinergic and muscarinic receptors, respectively.

250 Genetic deletion of muscarinic receptors resulted in significantly diminishe

251 ffects on prominent events downstream of the muscarinic receptor second messengers diacylglycerol (de

252 y and underlie the K(+) current sensitive to muscarinic receptor signaling (the M current) in sympath

253 Endothelial-dependent muscarinic receptor signaling also acted largely through

254 Carbachol (CCh), a muscarinic receptor-specific agonist, abrogated tumor ne

255 sal striatum and pharmacological blockade of muscarinic receptors, specifically postsynaptic M1 and M

256 um nitroprusside was ultimately dependent on muscarinic receptor stimulation as all effects were bloc

257 SS use secretagogues to induce secretion via muscarinic receptor stimulation.

258 and docking studies based on recently solved muscarinic receptor structures, further support the defi

259 tanding of the potential that members of the muscarinic receptor subtype family hold as therapeutic d

260 However, the specific muscarinic receptor subtype involved and the critical in

261 ted the hypothesis that the lack of a single muscarinic receptor subtype leads to age-dependent neuro

262 There are five muscarinic receptor subtypes (M1R to M5R), which, despit

263 striatal cholinergic interneurons (ChIs) and muscarinic receptor subtypes (mAChRs) in the occurrence

264 Mutational modification of distinct muscarinic receptor subtypes has yielded novel designer

265 s, due to indiscriminate activation of other muscarinic receptor subtypes, are common.

266 Of the five muscarinic receptor subtypes, the M5 receptor is the onl

267 ating agents show high affinity for all five muscarinic receptor subtypes, thus increasing the likeli

268 rthosteric binding pocket at any of the five muscarinic receptor subtypes.

269 ckers that have little or no effect on other muscarinic receptor subtypes.

270 provide the initial activation of MLCK with muscarinic receptors supporting sustained responses.

271 ion releases presynaptic gating through M(1) muscarinic receptors that downregulate adenosine inhibit

272 this notion, we find that sAHP inhibition by muscarinic receptors that increase phosphoinositide turn

273 Monomers and oligomers of the M2 muscarinic receptor therefore have been compared to iden

274 nese hamster ovary cells that expressed M(3) muscarinic receptors; this enhancement was observed for

275 tylcholine release at these synapses allowed muscarinic receptors to faithfully encode physiological

276 hin the orthosteric pockets of M(1) and M(2) muscarinic receptors to identify where acetylcholine mus

277 carbachol and that these agents act through muscarinic receptors to induce pigment granule dispersio

278 We find that the ability of muscarinic receptors to induce the inward aftercurrent u

279 ACh then activates MAPK/ERK via muscarinic receptors to promote neurite outgrowth.

280 1 cascade plays a key role in the ability of muscarinic receptors to signal the inward aftercurrent.

281 In both cell types activation of their muscarinic receptors triggers a general increase of exci

282 rough distinct actions at both nicotinic and muscarinic receptors, triggers a procession of neural os

283 ium-dependent vasodilatations in response to muscarinic receptor, TRPV4 (transient receptor potential

284 vasodilatations in response to activation of muscarinic receptors, TRPV4 channels or IK/SK channels w

285 n's Syndrome (SS) and HCV, presence of anti- muscarinic receptor type 3 (M3R) antibodies in SS, the r

286 Here we show that muscarinic receptor type-1 (Chrm1) signaling in the hypo

287 erved in principal neurons were dependent on muscarinic receptors type 1, engaging different intracel

288 One pathway shown for KCNQ2 and muscarinic receptors uses PKC, recruited to the channels

289 Thus, during submaximal activation of muscarinic receptors, V(m) can modulate Ca(2+) entry thr

290 ed previously that amiodarone interacts with muscarinic receptors via a novel allosteric site.

291 Stimulation of the M(3)-muscarinic receptor was shown to inhibit the ability of

292 t a classical G(q/11)-coupled GPCR, the M(3)-muscarinic receptor, was able to regulate apoptosis thro

293 tructure-based docking against the M2 and M3 muscarinic receptors, we screened 3.1 million molecules

294 To study the role of cochlear muscarinic receptors, we studied receptor localization w

295 ed monomers and tetramers of the purified M2 muscarinic receptor were compared with muscarinic recept

296 M2 immunoreactivity and M3 mRNA levels of muscarinic receptor were increased at day 7.

297 By focusing on muscarinic receptors, which are activated by the nerve-d

298 ral GPCRs, including beta2-adrenergic and M2 muscarinic receptors, which are commonly used as represe

299 anced calcium mobilization after stimulating muscarinic receptors with carbachol and after stimulatin

300 reatment of cells expressing either m1 or m3 muscarinic receptors with methyl-beta-cyclodextrin produ