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-A inhibits odor responses and is localized in Keny

3 mAChR-mediated enhancement of GABA release also presynap

4 mAChRs are often preferentially distributed on specializ

5 M(1) mAChR activation induced long-term depression at inputs

6 We found that systemic M(1) mAChR antagonism impaired contextual fear extinction.

7 y is necessary for fear extinction, and M(1) mAChR function is required for proper contextual fear ex

8 ldtype mice, rats, and NHPs, but not in M(1) mAChR KO mice, VU0453595 produced dose-related increases

9 gh (range, 10-81 mL/cm(3)) in all known M(1) mAChR-rich brain regions.

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

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

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

13 M(1) mAChRs dynamically modulate synaptic transmission at two

14 ical tools to assess the involvement of M(1) mAChRs in conditioned fear extinction in control mice an

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

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

17 Docking simulations on the M(3) mAChR-resolved structure rationalized the experimental o

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

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

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

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

22 and studied for their affinity at M(1)-M(5) mAChRs.

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

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

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

26 cated ticks, while injection of atropine, an mAChR-A antagonist, did not show any effect on water vol

27 2 (QR2) to be expressed in the cortex in an mAChR-dependent manner.

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

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

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

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

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

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

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

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

36 We pharmacologically assessed mAChR-A to monitor intracellular calcium mobilization up

37 321 binding affinity was >300-fold higher at mAChR and 29-fold higher at beta(2)AR relative to its mo

38 anism consistent with competitive binding at mAChRs.

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

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

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

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

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

44 oxical ChI excitation, which was reversed by mAChR inhibition.

45 nd depression of striatal DA transmission by mAChR agonists.

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

47 tribute to the suppression of BK channels by mAChRs.

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

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

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

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

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

53 affinities or binding kinetics for different mAChR subtypes.

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

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

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

57 vioral and theta state as well as endogenous mAChR activation.

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

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

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

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

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

63 subtype-selective allosteric modulators for mAChRs has provided an unprecedented opportunity for hig

64 y in the 6-position, showed pK(i) values for mAChRs higher than those of 2 and a selectivity profile

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

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

67 However, mAChR allosteric modulators can display a diverse array

68 If mAChR-dependent EPF selectively supports transient memor

69 of bivalent and linker-attached compounds in mAChRs.

70 ecific modulation of signaling by individual mAChR subtypes in the brain.

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

72 RPa inhibits BAT SNA via activation of local mAChR.

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

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

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

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

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

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

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

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

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

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

83 tool for pharmacological investigation of M1 mAChR PAMs.

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

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

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

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

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

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

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

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

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

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

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

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

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

97 ken together, these data suggest that the M1 mAChR may be a novel target for the pharmacological enha

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

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

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

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

102 in molecular dynamics simulations of the M1 mAChR than in those of other mAChRs.

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

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

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

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

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

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

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

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

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

112 gues designed to bind irreversibly to the M1 mAChR.

113 nd retained exquisite selectivity for the M1 mAChR.

114 tified 14 sites of phosphorylation on the M1 mAChR.

115 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

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

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

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

119 1 mAChRs, we show that once internalized, M1 mAChRs traffic to early endosomes, recycling endosomes a

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

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

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

123 positive allosteric modulators (PAMs) of M1 mAChRs.

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

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

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

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

128 switch into the molecular structure of an M2 mAChR agonist.

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

130 PAI enables light-dependent activation of M2 mAChRs.

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

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

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

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

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

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

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

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

145 tivation and beta-arrestin2 engagement at M4 mAChR.

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

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

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

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

150 119620 binds allosterically to the M2 and M4 mAChRs and was positively cooperative with muscarinic or

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

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

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

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

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

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

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

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

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

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

161 ptic tectum showed expression of one or more mAChRs.

162 Moreover, mAChR-A knockdown impairs the learning-associated depres

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

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

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

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

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

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

169 electrophysiology, we assessed the effect of mAChR activation on the synaptic strength of specific PF

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

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

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

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

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

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

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

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

178 cial for rWTX interactions with all types of mAChR.

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

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

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

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

183 his mechanism is under modulatory control of mAChRs.

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

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

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

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

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

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

190 sed to selectively activate either nAChRs or mAChRs.

191 tions of the M1 mAChR than in those of other mAChRs.

192 previously characterized modulators of other mAChRs.

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

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

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

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

197 not by subthreshold depolarization preceding mAChR stimulation.

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

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

200 We show that PSC mAChR-dependent activity was transiently increased at di

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

202 Recently, mAChR allosteric modulators have entered clinical develo

203 of the M1 muscarinic acetylcholine receptor (mAChR) achieve exquisite selectivity by occupying a dyna

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

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

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

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

208 es of the muscarinic acetylcholine receptor (mAChR) antagonist 2 was synthesized and studied for thei

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

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

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

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

213 systemic muscarinic acetylcholine receptor (mAChR) inhibition.

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

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

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

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

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

219 The M(1) muscarinic acetylcholine receptor (mAChR) plays an important role in learning and memory, a

220 M(1) muscarinic acetylcholine receptor (mAChR) positive allosteric modulators (PAMs) have been r

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

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

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

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

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

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

227 a form of muscarinic acetylcholine receptor (mAChR)-dependent long-term depression in the PFC that we

228 of the M1 muscarinic acetylcholine receptor (mAChR).

229 at the M1 muscarinic acetylcholine receptor (mAChR).

230 at the M1 muscarinic acetylcholine receptor (mAChR).

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

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

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

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

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

236 Muscarinic acetylcholine receptors (mAChR) play important roles in regulating complex behavi

237 s type A muscarinic acetylcholine receptors (mAChR-A), particularly in the gamma subtype of Kenyon ce

238 3 and M2 muscarinic acetylcholine receptors (mAChRs) and beta-2-adrenoceptors (beta2ARs) are importan

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

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

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

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

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

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

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

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

247 ition of muscarinic acetylcholine receptors (mAChRs) reduced calcium activity while increasing SWRs.

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

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

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

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

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

253 nd B) of muscarinic acetylcholine receptors (mAChRs), which were expressed in Ixodes SG.

254 cts with muscarinic acetylcholine receptors (mAChRs).

255 ation by muscarinic acetylcholine receptors (mAChRs).

256 through muscarinic acetylcholine receptors (mAChRs).

257 known as muscarinic acetylcholine receptors (mAChRs).

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

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

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

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

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

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

264 nvolve the muscarinic cholinergic receptors (mAChRs).

265 Indeed, muscarinic receptors (mAChRs) regulate the repair phenotype of PSCs and are ov

266 s caused by overactive muscarinic receptors (mAChRs), leading to a switch in D2R coupling from canoni

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

268 dverse effects associated with non-selective mAChR agonists.

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

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

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

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

273 Systemic mAChR blockade attenuated Th17 activity and enhanced Th2

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

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

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

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

278 Our results suggest that mAChR-A function in Kenyon cell dendrites is required fo

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

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

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

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

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

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

285 of control tests suggests the effects of the mAChR antagonists were sensitive to changes in reward va

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

287 ies, and a more nuanced understanding of the mAChR will be necessary to best translate preclinical fi

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

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

290 rgic neurons in the ventral ganglion through mAChR.

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

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.