ライフサイエンスコーパス: mAChR

1 mAChR activation reduces the Ca sensitivity of small con

2 mAChR-mediated enhancement of GABA release also presynap

3 mAChRs are often preferentially distributed on specializ

4 rovide strong support for targeting the M(1) mAChR as a therapeutic candidate in AD.

5 These results indicate that the M(1) mAChR is an important regulator of amyloidogenesis in th

6 In this study, we used M(1) mAChR knock-out mice (M(1)KO) to isolate the effects of

7 (M(1)KO) to isolate the effects of the M(1) mAChR on APP processing in primary neurons and on the de

8 94), lost agonistic selectivity for the M(1) mAChR.

9 ric site and an allosteric site, at the M(1) mAChR.

10 ecedented functional selectivity at the M(1) mAChR.

11 rescued this phenotype, indicating that M(1) mAChRs are sufficient to modulate nonamyloidogenic APP p

12 We demonstrate that the loss of M(1) mAChRs increases amyloidogenic APP processing in neurons

13 brain tissue indicates that the loss of M(1) mAChRs increases amyloidogenic APP processing.

14 Expression of M(1) mAChRs on the M(1)KO background rescued this phenotype,

15 P(Swe/Ind) transgenic mice, the loss of M(1) mAChRs resulted in increased levels of brain Abeta and g

16 how that LY2033298 can also bind to the M(2) mAChR and mediate robust positive or negative allosteric

17 kinase 1/2 phosphorylation assay at the M(2) mAChR revealed that, although the effects on binding wer

18 Like other mAChR subtypes, the M(4) mAChR is widely expressed in different regions of the fo

19 ate the physiological relevance of this M(4) mAChR subpopulation in modulating dopamine-dependent beh

20 ly potentiate the actions of ACh at the M(4) mAChR subtype.

21 Interestingly, M(4) mAChRs are coexpressed with D(1) dopamine receptors in a

22 ology to generate mutant mice that lack M(4) mAChRs only in D(1) dopamine receptor-expressing cells.

23 copolamine at the M(1), M(2), M(3), and M(4) mAChRs revealed radioligand displacement in a manner con

24 ed to as muscarinic ACh receptors (M(1)-M(5) mAChRs).

25 o trace or delay conditioning, with either a mAChR antagonist (scopolamine) or saline.

26 In contrast to PV BCs, CCK BCs exhibited a mAChR-induced afterdepolarization (mADP) that was freque

27 ts transient memory, then blocking amygdalar mAChRs should impair trace conditioning, while sparing d

28 present study examined the role of amygdalar mAChRs in trace fear conditioning, a paradigm that requi

29 2 (QR2) to be expressed in the cortex in an mAChR-dependent manner.

30 The effects of nAChR and mAChR activation on HC currents and zero electrode curre

31 We visualize PV- and mAChR-immunoreactive somata by dual-immunofluorescence c

32 ects of desiccating environmental stress and mAChR inhibition on the pathogenesis of DED.

33 ion in spinal cord slices from wild-type and mAChR subtype knock-out (KO) mice.

34 n spinal cord slices from wild-type (WT) and mAChR subtype knock-out (KO) mice.

35 understand the interaction between AEME and mAChRs and how it can lead to neuronal death.

36 ible interactions between group I mGluRs and mAChRs in anti-Hebbian LTP at synapses which excite orie

37 The clinical effectiveness of some anti-mAChR drugs in treating motion sickness suggest that we

38 expressed in the rabbit retina and to assess mAChR distribution and the functional effects of mAChR a

39 THRX-198321 was a competitive antagonist at mAChR (M(2) pK(B) = 9.98 +/- 0.13; M(3) pK(B) = 10.31 +/

40 321 binding affinity was >300-fold higher at mAChR and 29-fold higher at beta(2)AR relative to its mo

41 anism consistent with competitive binding at mAChRs.

42 Cross-regulation or crosstalk between mAChRs and beta2ARs in airway smooth muscle (ASM) helps

43 onal significance of the interaction between mAChRs and KARs we examined the effect of mAChR activati

44 rgic transmission pharmacologically blocked, mAChR activation enhanced PV cell excitability in both C

45 This excitation is followed by mAChR-mediated inhibition, which is blocked by GABAA rec

46 The inhibition of BAT SNA mediated by mAChR in rRPa does not depend on activation of GABA rece

47 nd depression of striatal DA transmission by mAChR agonists.

48 A signaling pathway triggered by mAChR activation is the production and release of endoca

49 tribute to the suppression of BK channels by mAChRs.

50 followed by inhibition mediated directly by mAChRs on PGCs/SACs.

51 e modulated in a subunit dependent manner by mAChRs.

52 rt, no therapeutic agents endowed with clear mAChR subtype selectivity have been developed to exploit

53 is results from the activation of Gq-coupled mAChRs present on Purkinje cells.

54 al structure but not by previously described mAChR allosteric compounds such as gallamine or WIN 62,5

55 In this review we will detail mAChR and beta2AR-signaling and crosstalk, focusing on e

56 affinities or binding kinetics for different mAChR subtypes.

57 ighly selective activators for the different mAChR and nAChR subtypes with suitable properties for op

58 However, it is not clear how each mAChR subtype contributes to the regulation of glutamate

59 However, it is unclear how each mAChR subtype regulates excitatory synaptic input from p

60 stochemical analyses confirmed that all five mAChR subtypes were expressed by subpopulations of bipol

61 inds directly and selectively to one of five mAChR subtypes, M4 receptors (M4Rs), at their C-terminal

62 Although the five mAChR subtypes (M1-M5) share a high degree of sequence h

63 The increase in BAT SNA following mAChR blockade in rRPa does not depend on the activity o

64 THRX-198321 exhibited high affinity for mAChR (M(2) pK(I,App) = 10.57 +/- 0.09; M(3) pK(I,App) =

65 be the case for other selective agonists for mAChRs, and should be taken into consideration in the pr

66 selective ligand design and development for mAChRs and facilitate improved identification of bitopic

67 Selective activation of glomerular mAChRs in the presence of tetrodotoxin increased IPSCs i

68 Indeed, selective activation of glomerular mAChRs, with ionotropic GluRs and nAChRs blocked, increa

69 Within the hippocampus, mAChRs promote NMDA-type glutamate receptor-dependent fo

70 If mAChR-dependent EPF selectively supports transient memor

71 cholinergic response profiles, differing in mAChR-induced changes in action potential (AP) waveform,

72 of bivalent and linker-attached compounds in mAChRs.

73 Instead, mAChRs modulate a negative feedback loop in spines that

74 ons, whereas corticocallosal neurons lacking mAChR-mediated depolarizing potentials did not show pers

75 RPa inhibits BAT SNA via activation of local mAChR.

76 moral activation of asymmetrically localized mAChRs by ACh is an evolutionarily conserved mechanism b

77 M1 mAChR internalization is both beta-arrestin and G protei

78 ntly increased at a constitutively active M1 mAChR but abolished at an inactive mutant.

79 ChR and alcohol 5c behaved much like 3 at M1 mAChR and showed full antagonism in both Gi activation a

80 ition thereby establishing a link between M1 mAChR activation and hippocampus-based memory and learni

81 However, developing M1 mAChR-selective orthosteric ligands has proven challengi

82 ion of M1 mAChRs from PV cells diminished M1 mAChR immunoreactivity and muscarinic excitation of HC P

83 Saturation analysis of a human M1 mAChR stable cell line showed that [(3)H]PT-1284 bound t

84 efficacy for beta-arrestin2 engagement in M1 mAChR and alcohol 5c behaved much like 3 at M1 mAChR and

85 orylation at Ser(228) was an indicator of M1 mAChR activation.

86 and characterization of a novel family of M1 mAChR PAMs.

87 tool for pharmacological investigation of M1 mAChR PAMs.

88 be exploited to tailor the development of M1 mAChR-targeting PAMs.

89 udy we investigated the impact of BQCA on M1 mAChR regulation.

90 s benzoquinazolinone 12) as a more potent M1 mAChR PAM with a structural ancestry originating from BQ

91 c agonist xanomeline (1) and the putative M1 mAChR allosteric agonist 1-[3-(4-butylpiperidin-1-yl)pro

92 the M1 muscarinic acetylcholine receptor (M1 mAChR) are a promising strategy for the treatment of the

93 the M1 muscarinic acetylcholine receptor (M1 mAChR) in vitro and in vivo Mass spectrometry phosphopro

94 the M1 muscarinic acetylcholine receptor (M1 mAChR), which was previously shown to have procognitive

95 etained functional activity at the target M1 mAChR and D2R and demonstrated high affinity for the 5-H

96 rmining the phosphorylation status of the M1 mAChR at Ser(228) not only provides a means of establish

97 e mapping of the activation status of the M1 mAChR in the hippocampus following memory acquisition th

98 ication of phosphorylated Ser(228) on the M1 mAChR in the hippocampus of mice following administratio

99 The M1 mAChR is an attractive target for the cognitive deficits

100 Moreover, docking simulations on the M1 mAChR model were performed to elucidate how the binding

101 g of the interaction between TBPB and the M1 mAChR revealed a binding pose predicted to extend from t

102 serine at position 228 (Ser(228)) on the M1 mAChR showed extremely low levels of basal phosphorylati

103 e report that selective activation of the M1 mAChR subtype induces LTD in PFC and that this response

104 ular dynamics to delineate regions of the M1 mAChR that govern modulator binding and transmission of

105 c modulator and allosteric agonist at the M1 mAChR that has high subtype selectivity and is a promisi

106 response, consistent with studies of the M1 mAChR with the prototypical PAM, BQZ12.

107 tribute to the BQCA binding pocket at the M1 mAChR, as well as to the transmission of cooperativity w

108 Despite having a low affinity for the M1 mAChR, BQCA demonstrated state dependence, exhibiting hi

109 ite in the extracellular vestibule of the M1 mAChR, suggesting that its high subtype selectivity deri

110 In addition, the M1 mAChR-positive allosteric modulator, 1-(4-methoxybenzyl)

111 ; ideally, by co-crystallization with the M1 mAChR.

112 ar basis for its improved activity at the M1 mAChR.

113 gues designed to bind irreversibly to the M1 mAChR.

114 nd retained exquisite selectivity for the M1 mAChR.

115 tified 14 sites of phosphorylation on the M1 mAChR.

116 l line showed that [(3)H]PT-1284 bound to M1 mAChR in the presence of 1 mM ACh with Kd, 4.23 nM, and

117 ng hippocampal muscarinic signaling using M1 mAChR PAMs restored memory loss and slowed the progressi

118 s on activation of both group I mGluR and M1 mAChRs.

119 To delete M1 mAChRs genetically from PV interneurons, we created PV-M

120 1 mAChRs, we show that once internalized, M1 mAChRs traffic to early endosomes, recycling endosomes a

121 The elimination of M1 mAChRs from PV cells diminished M1 mAChR immunoreactivit

122 Therefore, the direct activation of M1 mAChRs on PV cells contributes to some forms of learning

123 h to monitor intracellular trafficking of M1 mAChRs, we show that once internalized, M1 mAChRs traffi

124 positive allosteric modulators (PAMs) of M1 mAChRs.

125 that blockade of either group I mGluRs or M1 mAChRs prevented the induction of anti-Hebbian LTP by pa

126 neficial effects by blocking postsynaptic M1 mAChRs expressed on medium spiny neurons (MSNs) at the o

127 C excitability was altered solely through M1 mAChRs.

128 nist-induced beta-arrestin recruitment to M1 mAChRs.

129 ed that the rWTX loop II protrudes to the M1-mAChR allosteric ligand-binding site blocking the entran

130 lator of agonist-mediated response at the M2 mAChR.

131 nist N-methylscopolamine to human M1- and M2-mAChRs, and increased antagonist binding to M3-mAChR.

132 here the structure of the G(q/11)-coupled M3 mAChR ('M3 receptor', from rat) bound to the bronchodila

133 e to the partial agonist effect at M1 and M3 mAChRs, leading to DNA fragmentation and neuronal death

134 without significant effect at the M1 and M3 mAChRs.

135 , the interaction between postsynaptic M1/M3 mAChRs and endocannabinoid signaling is input specific,

136 inated with simultaneous activation of M1/M3 mAChRs, anti-Hebbian LTD is induced.

137 unction data converged on the presence of M3 mAChRs in distinguishing CCK BCs from PV BCs.

138 equency of CCK BCs was controlled through M3 mAChRs but PV BC excitability was altered solely through

139 eered mouse expressing a G protein-biased M3-mAChR mutant, we reveal the first evidence, to our knowl

140 iological responses that are regulated by M3-mAChR phosphorylation (which include control of lung fun

141 evidence, to our knowledge, of a role for M3-mAChR phosphorylation in bronchial smooth muscle contrac

142 the physiological/therapeutic outcome of M3-mAChR-biased ligands with important implications for dru

143 the M3-muscarinic acetylcholine receptor (M3-mAChR).

144 ChRs, and increased antagonist binding to M3-mAChR.

145 In contrast, toxin interacts with M3-mAChR by loop II without penetration into the allosteric

146 al administration of the selective M1 and M4 mAChR antagonists telenzepine and tropicamide, respectiv

147 tivation and beta-arrestin2 engagement at M4 mAChR.

148 ]pyridine carboxamide), bind to the human M4 mAChR allosteric pocket.

149 were unsuccessful because of the lack of M4 mAChR subtype specificity and off-target muscarinic adve

150 amide, to reduce the activity through the M4 mAChR and investigated the behavioral response in the Fm

151 The M4 mAChR is implicated in several CNS disorders and possess

152 119620 binds allosterically to the M2 and M4 mAChRs and was positively cooperative with muscarinic or

153 tered cholinergic transmission via M1 and M4 mAChRs of the dorsal striatum plays a pivotal role in th

154 ceptors, specifically postsynaptic M1 and M4 mAChRs, alleviate lesion-induced motor deficits.

155 to the same allosteric site on the human M4 mAChRs.

156 olished in mutant lesioned mice that lack M4 mAChRs specifically in dopamine D1-receptor-expressing n

157 We also show that M2/M4 mAChRs depress the nAChR-dependent mechanism of DA relea

158 ing neurons, suggesting that postsynaptic M4 mAChRs expressed on direct MSNs mediate the antiakinetic

159 ant cell line stably expressing the human M5 mAChR, we investigated the effects of the positive allos

160 at novel small-molecule modulators of the M5 mAChR display mixed mechanisms of action compared with p

161 ication of mRNA transcripts for the m1 to m5 mAChR subtypes.

162 We found that M5 mAChRs potentiate DA and glutamate release only from DA

163 In wild-type mice, mAChR activation with oxotremorine-M decreased the ampli

164 ptic tectum showed expression of one or more mAChRs.

165 ounds mediate their actions in CAR via a non-mAChR-mediated mechanism.

166 vels of mGluR1 activation on a background of mAChR agonists may be able to initiate alpha activity th

167 This modulatory capacity of mAChR signaling could promote the functional penetrance

168 ptor, offers possibilities for the design of mAChR subtype-selective ligands.

169 iling suggested that despite being devoid of mAChR M2/M3 subtype activity, compound 38 still carries

170 en mAChRs and KARs we examined the effect of mAChR activation on KAR-mediated excitotoxicity.

171 r suggest that the clinical effectiveness of mAChR antagonists in treating balance disorders may also

172 R distribution and the functional effects of mAChR activation and blockade on retinal response proper

173 The expression of mAChR subtypes on subsets of bipolar, amacrine, and gang

174 Our findings clarify the mechanisms of mAChR-dependent modulation of DA and glutamate transmiss

175 By contrast, in our model of mAChR-induced alpha, TC cells tend to fire either at the

176 nists and positive allosteric modulators, of mAChR and nAChR subtypes demonstrate unique mechanisms o

177 Thus, the overall pattern of mAChR expression found is in agreement with mAChR expres

178 rthosteric and allosteric binding pockets of mAChR and beta(2)AR, a phenomenon that may be unique to

179 regions in neurons, but the significance of mAChR localization in modulating neuronal function is no

180 gment (BA-L) binds to the allosteric site of mAChR (M(2) pEC(50,diss) = 5.06 +/- 0.03; M(3) pEC(50,di

181 cial for rWTX interactions with all types of mAChR.

182 Exogenous activation of mAChRs led to LTP, with changes in EPSP amplitude distri

183 e V(z) in type I pigeon HCs by activation of mAChRs represents a new finding.

184 Brief activation of mAChRs with pilocarpine significantly enhances KAR-media

185 the effects of the activation or blockade of mAChRs on ganglion cell response properties.

186 Coactivation of mAChRs and mGluRs also induced a long-lasting enhancemen

187 ndertaken to identify the full complement of mAChRs expressed in the rabbit retina and to assess mACh

188 his mechanism is under modulatory control of mAChRs.

189 identify the complement and distribution of mAChRs in the rabbit retina.

190 is elegans homolog of the M1/M3/M5 family of mAChRs, gar-3, is expressed in cholinergic motor neurons

191 In addition, drugs enhancing the function of mAChRs are used to treat memory impairment and decline.

192 derstanding the distribution and function of mAChRs in the retina has the potential to provide import

193 In vivo inhibition of mAChRs variably affects CD4(+) T-cell subsets, and desic

194 the target-specific allosteric regulation of mAChRs by "three-finger" snake neurotoxins.

195 The functional roles of mAChRs in glomerular circuits are unknown.

196 ns of THRX-198321 with an allosteric site on mAChR and a novel extracellular allosteric site on beta(

197 sed to selectively activate either nAChRs or mAChRs.

198 Like other mAChR subtypes, the M(4) mAChR is widely expressed in di

199 previously characterized modulators of other mAChRs.

200 tudies have provided evidence for overactive mAChR signaling in the fragile X knock-out (Fmr1KO) mous

201 at RMPs were immediately rescued by pairing mAChR stimulation with subthreshold depolarization ( app

202 o our knowledge the effects of pharmacologic mAChR blockade on the pathogenesis of experimental DED h

203 )AR (pK(I,App) = 9.54 +/- 0.15), with potent mAChR antagonist (M(2) pK(I,Fn) = 9.69 +/- 0.23; M(3) pK

204 not by subthreshold depolarization preceding mAChR stimulation.

205 It was found that presumed mAChR activation decreased both inward and outward curre

206 tion models to investigate which presynaptic mAChR subtype mediates the antipsychotic-like effects of

207 icocallosal neurons, ACh generated prolonged mAChR-mediated depolarizing potentials in corticocollicu

208 ditionally, we assessed AEME activity at rat mAChR subtypes 1-5 heterologously expressed in Chinese H

209 diated by muscarinic acetylcholine receptor (mAChR) activation and the subsequent closure of KCNQ pot

210 Muscarinic acetylcholine receptor (mAChR) activation in rRPa contributes to the inhibition

211 ngaged by muscarinic acetylcholine receptor (mAChR) activation.

212 ective M4 muscarinic acetylcholine receptor (mAChR) activators may offer a novel strategy for the tre

213 ns of the muscarinic acetylcholine receptor (mAChR) agonist, oxotremorine, or the cholinesterase inhi

214 osed of a muscarinic acetylcholine receptor (mAChR) antagonist moiety, represented by the fragment MA

215 Muscarinic acetylcholine receptor (mAChR) blockade by scopolamine produces similar anti-par

216 of the M5 muscarinic acetylcholine receptor (mAChR) have been described, but their molecular mechanis

217 ubtype of muscarinic acetylcholine receptor (mAChR) in the prefrontal cortex (PFC) and also display i

218 systemic muscarinic acetylcholine receptor (mAChR) inhibition.

219 of the M1 muscarinic acetylcholine receptor (mAChR) is a prospective treatment for alleviating cognit

220 of the M2 muscarinic acetylcholine receptor (mAChR) is targeted for structure-based design of alloste

221 the first muscarinic acetylcholine receptor (mAChR) negative allosteric modulator (NAM) selective for

222 of either muscarinic acetylcholine receptor (mAChR) or metabotropic glutamate receptor 1 (mGluR1) ago

223 the M1/M4 muscarinic acetylcholine receptor (mAChR) orthosteric agonist xanomeline (1) and the putati

224 terized a muscarinic acetylcholine receptor (mAChR) potentiator, LY2119620 (3-amino-5-chloro-N-cyclop

225 M) of the muscarinic acetylcholine receptor (mAChR) subtype 5 (M5).

226 ration of muscarinic acetylcholine receptor (mAChR) subtype-selective compounds has been challenging,

227 of the M1 muscarinic acetylcholine receptor (mAChR) that may gain their selectivity through a bitopic

228 of the M1 muscarinic acetylcholine receptor (mAChR) via a positive allosteric modulator (PAM) is a ne

229 or the M1 muscarinic acetylcholine receptor (mAChR), but it possesses low affinity for the allosteric

230 of the M1 muscarinic acetylcholine receptor (mAChR).

231 at the M1 muscarinic acetylcholine receptor (mAChR).

232 at the M1 muscarinic acetylcholine receptor (mAChR).

233 it requires ACh and muscarinic ACh receptor (mAChR) activation.

234 zing potentials and muscarinic ACh receptor (mAChR)-mediated hyperpolarizing potentials in AC L5B cor

235 (1) muscarinic acetylcholine (ACh) receptor (mAChR) has led to the discovery of various selective ago

236 dy, we determined which muscarinic receptor (mAChR) subtypes are present in the brain of Apteronotus

237 Muscarinic acetylcholine receptors (mAChR) are G protein-coupled receptors (M1-M5), grouped

238 ckade of muscarinic acetylcholine receptors (mAChRs) affects retinal ganglion cell light responses an

239 3 and M2 muscarinic acetylcholine receptors (mAChRs) and beta-2-adrenoceptors (beta2ARs) are importan

240 ation of muscarinic acetylcholine receptors (mAChRs) and is triggered by suprathreshold stimulation.

241 Although muscarinic acetylcholine receptors (mAChRs) and NMDA receptors (NMDARs) are important for sy

242 hRs) and muscarinic acetylcholine receptors (mAChRs) are expressed in glomeruli.

243 Muscarinic acetylcholine receptors (mAChRs) are known to modulate synaptic plasticity in var

244 Muscarinic acetylcholine receptors (mAChRs) are widely expressed in the mammalian brain and

245 ation of muscarinic acetylcholine receptors (mAChRs) controls the size and sign of associative long-t

246 ation of muscarinic acetylcholine receptors (mAChRs) has been shown to affect APP processing and AD p

247 , by the muscarinic acetylcholine receptors (mAChRs) in relevant brain structures.

248 ation of muscarinic acetylcholine receptors (mAChRs) in the spinal cord inhibits pain transmission.

249 ation of muscarinic acetylcholine receptors (mAChRs) inhibits nociceptive transmission at the spinal

250 M(1) muscarinic acetylcholine receptors (mAChRs) represent a viable target for treatment of multi

251 tum, and muscarinic acetylcholine receptors (mAChRs) share some signaling pathways and cooperate with

252 ation of muscarinic acetylcholine receptors (mAChRs) significantly increased the amplitude of both un

253 uRs) and muscarinic acetylcholine receptors (mAChRs) synergistically increase the excitability of hip

254 modified muscarinic acetylcholine receptors (mAChRs) that have minimal responsiveness to acetylcholin

255 ation by muscarinic acetylcholine receptors (mAChRs).

256 through muscarinic acetylcholine receptors (mAChRs).

257 known as muscarinic acetylcholine receptors (mAChRs).

258 cts with muscarinic acetylcholine receptors (mAChRs).

259 controversial how muscarinic ACh receptors (mAChRs) modulate striatal DA release, with studies repor

260 rs (nAChRs) and M2 muscarinic ACh receptors (mAChRs), respectively.

261 and nicotinic acetylcholine (ACh) receptors (mAChRs and nAChRs) are emerging as important targets for

262 pe muscarinic acetylcholine (ACh) receptors (mAChRs) mediate two distinct electrophysiological respon

263 pe muscarinic acetylcholine (ACh) receptors (mAChRs) mediate two distinct electrophysiological respon

264 4) muscarinic acetylcholine (ACh) receptors (mAChRs) on the basis of its ability to preferentially po

265 ivation of muscarinic cholinergic receptors (mAChRs) enhance synaptic plasticity in vitro and cogniti

266 nvolve the muscarinic cholinergic receptors (mAChRs).

267 nicotinic (nAChRs) and muscarinic receptors (mAChRs), are expressed by vestibular hair cells (VHCs).

268 While early attempts to develop selective mAChR and nAChR agonists provided important preliminary

269 dverse effects associated with non-selective mAChR agonists.

270 strong evidence that activators of specific mAChR (M(1) and M(4)) and nAChR (alpha(7) and alpha(2)be

271 ut less is known about the roles of specific mAChR subtypes.

272 In response to depolarizing current steps, mAChR activation of PV BCs and CCK BCs also elicited dis

273 g calcium release from intracellular stores, mAChR activation facilitates voltage-dependent refilling

274 ons (ChIs) and muscarinic receptor subtypes (mAChRs) in the occurrence of a wide range of motor defic

275 Systemic mAChR blockade attenuated Th17 activity and enhanced Th2

276 esiccating environmental stress and systemic mAChR blockade induce DED through different primary path

277 esiccating environmental stress and systemic mAChR blockade induced similar clinical signs of DED.

278 Th17-cell activity and Treg dysfunction than mAChR blockade, while mAChR blockade decreased tear secr

279 Finally, we demonstrate that mAChR activation inhibits L-type Ca channels and thus ma

280 We suggest that mAChR-induced alpha may contribute to grouping TC activi

281 s to mechanical stimulation, suggesting that mAChR activation increases afferent input impedance by c

282 Our results demonstrate that mAChRs in CWC spines act by suppressing large-conductanc

283 ased IPSCs in MTCs and ETCs, indicating that mAChRs recruit glomerular inhibitory circuits.

284 This study investigates the mAChR-mediated regulation of release from three types of

285 Nanoinjections of the mAChR antagonist, scopolamine (SCOP), in the rRPa of war

286 To decipher which of the mAChR subtypes provides these beneficial effects, system

287 However, in contrast to the mAChR-mediated hyperpolarizing potentials in corticocall

288 At least three mAChR subtypes (M(2), M(3), and M(4)) are present in the

289 rgic neurons in the ventral ganglion through mAChR.

290 In addition, ACh can bind to mAChRs expressed near cholinergic release sites, resulti

291 Transient mAChR activation enhances this action of kainate, sugges

292 logy offer a unique opportunity to fine tune mAChR and beta2AR signaling and their crosstalk, and the

293 Finally, upon mAChR activation, glutamatergic transmission enhanced ce

294 sults suggest that cooperative signaling via mAChRs and group I mGluRs could provide a mechanism by w

295 Treg dysfunction than mAChR blockade, while mAChR blockade decreased tear secretion to a greater ext

296 etion of intracellular calcium stores, while mAChR-driven excitation acts to refill those stores by p

297 mAChR expression found is in agreement with mAChR expression in other species, with additional prese

298 insular cortex is inversely correlated with mAChR activation both endogenously, after novel taste le

299 ooperativity binding of [(3)H]LY2119620 with mAChR orthosteric agonists detects significant changes i

300 mirrors that of an ACh-bound wild-type (WT) mAChR.