ライフサイエンスコーパス: carbachol

1 e, high-K+ depolarization) and/or [Ca2+]cyt (carbachol).

2 n was slower for acetylcholine than that for carbachol.

3 ged for acetylcholine compared with that for carbachol.

4 ed by application of the cholinergic agonist carbachol.

5 ed with forskolin and a low concentration of carbachol.

6 ess in response to all other agonists except carbachol.

7 fected by cholinergic receptor activation by carbachol.

8 r isoproterenol but not increases induced by carbachol.

9 zation or in response to M3 receptor agonist Carbachol.

10 ogical treatment with the muscarinic agonist carbachol.

11 substantially reduced, but usually less than carbachol.

12 d in the presence of the muscarinic agonist, carbachol.

13 ite the continued perfusions of the STN with carbachol.

14 ors, elicited in response to brief pulses of carbachol.

15 sulted in inhibition of currents elicited by carbachol.

16 e increased when choline was co-applied with carbachol.

17 holinium-3 and restored by exogenously added carbachol.

18 is only approximately 60% of that seen with carbachol.

19 h (>500 nM) but not by low concentrations of carbachol.

20 l as MCCV increases produced by forskolin or carbachol.

21 on caused by the muscarinic receptor agonist carbachol.

22 myocytes treated with the muscarinic agonist carbachol.

23 very or prevented inhibition if added before carbachol.

24 or closely related synthetic analogs such as carbachol.

25 d does not support the inhibition of NHE3 by carbachol.

26 f cooperativity with the orthosteric agonist carbachol.

27 uired for the inhibition of NHE3 activity by carbachol.

28 o the plasma membrane after stimulation with carbachol.

29 ronotropic effects of the muscarinic agonist carbachol.

30 of oxygen saturation, and responsiveness to carbachol.

31 usiform cells using the cholinergic agonist, carbachol.

32 nsitivity to AF induction in the presence of carbachol.

33 tor protein CPI-17 were also stimulated with carbachol.

34 scle cells induced by the muscarinic agonist carbachol.

35 vity of beta-cells to the cholinergic analog carbachol.

36 tractile responses to the muscarinic agonist carbachol.

37 10 muM) and by the Ca(2+)-elevating agonist, carbachol (0.3 muM).

38 dialysis of the cholinergic receptor agonist carbachol (1 mM) into the STN caused an increase in the

39 a change from physiologic concentrations of carbachol (1 muM) to a supraphysiologic concentration (1

40 Following TTX application, carbachol (1 muM), substance P (1 muM) and an NKI agonis

41 , and stimulated with the muscarinic agonist carbachol (1 muM).

42 Stimulation (S1) with carbachol (10 microM) caused rapid, transient increases

43 the LH and the RVM, the cholinergic agonist carbachol (125 nmol) was microinjected into the LH of fe

44 brief application of the cholinergic agonist carbachol (25 microM) or elevated KCl in glucose-contain

45 ations throughout TM3 on the interactions of carbachol, 4-n-butyl-1-[4-(2-methylphenyl)-4-oxo-1-butyl

46 Using local photolysis of caged carbachol, a broad-spectrum cholinergic agonist, we mapp

47 al signal of taste novelty, in these studies carbachol, a direct cholinergic agonist, was infused int

48 Treatment of H508 cells with carbachol, a hydrolytically stable acetylcholine analog,

49 Carbachol, a known nAChR and muscarinic receptor agonist

50 ith type 3 muscarinic receptor (M3), we used carbachol, a ligand specific for muscarinic receptor, as

51 ty between BQCA and the orthosteric agonist, carbachol, across pathways.

52 Carbachol acted presynaptically by increasing the freque

53 o not alter its sensitivity to inhibition by carbachol acting through the Galphaq-11-PLCbeta signalin

54 The muscarinic receptor agonist carbachol activated ERK1/2 better in T1R3-depleted cells

55 Carbachol-activated TRPC5 currents were recorded by the

56 nstrate that the muscarinic receptor agonist carbachol activates AMPKalpha1-containing complexes in t

57 Adding carbachol after isoproterenol caused dissociated antegra

58 se display loss of potency for acetylcholine/carbachol alongside a concurrent gain in potency for the

59 Carbachol also increased the frequency of spontaneous ex

60 Co-stimulation with carbachol and 8-pCPT-2'-O-Me-cAMP led to an additive eff

61 M2R-IKACh signaling pathway in SAN cells to carbachol and a significant slowing of M2R-IKACh deactiv

62 ted in the RVM following LH stimulation with carbachol and abolished LH-induced antinociception as we

63 after stimulating muscarinic receptors with carbachol and after stimulating purinergic receptors wit

64 nse to common pharmacological agents such as carbachol and atropine but rarely form capillary-like st

65 The increase in [Ca2+]i caused by carbachol and BzATP used simultaneously was less than ad

66 mucosa inhibited ion transport responses to carbachol and forskolin but potentiated the reduced ion

67 In isolated islets, carbachol and PACAP/VIP synergistically promote beta-cel

68 The effects of high glucose on reactivity to carbachol and phenylephrine were determined.

69 gill retina with acetylcholine or its analog carbachol and that these agents act through muscarinic r

70 es across the tissues to the calcium agonist carbachol and the adenosine 3',5'-cyclic monophosphate a

71 educes the activation of the ARC channels by carbachol and, correspondingly, markedly inhibits the [C

72 o increase respiration in response to small (carbachol) and moderate (K(+) -depolarization) workloads

73 Secretagogues (cerulein, carbachol, and bombesin) can induce protease activation

74 CCK-8, carbachol, and bombesin, but not VIP/secretin, decreased

75 holine receptor activation by acetylcholine, carbachol, and other muscarinic agonists.

76 y of the full agonists, acetylcholine (ACh), carbachol, and oxotremorine-M, while significantly incre

77 the cholinergic agonists, acetylcholine and carbachol, and the cholinergic antagonists, D-tubocurari

78 Stimulation with cholecystokinin (CCK), carbachol, and vasoactive intestinal peptide all induced

79 on of NO-dependent signalling prevented both carbachol- and activity (5 Hz)-dependent LTD but not act

80 ne exemplified by orthosteric compounds like carbachol, another by structural analogs of AC-42, and a

81 Carbachol application had heterogeneous effects on neuro

82 SR-driven excitatory events was augmented by carbachol application.

83 exhibited a reduction in selectivity during carbachol application.

84 By injecting carbachol at the beginning of the light period or beginn

85 tractile or RLC phosphorylation responses to carbachol between tissues from normal mice vs. MYPT1 T85

86 All mutations tested severely reduced carbachol binding and activation of M(1).

87 n constants of 6 and 26 mM were obtained for carbachol binding to the A- and P-sites in E and of 2 an

88 e A- and P-sites in E and of 2 and 32 mM for carbachol binding to the A- and P-sites in EC.

89 Familiar taste-illness pairing following carbachol, but not vehicle, induced significant elevatio

90 phospholipase C inhibitor U-73122 abolished carbachol- but not forskolin-induced Rap1 activation.

91 3% showed evidence of a decreased potency of carbachol by a shift in the dose-response curve to the r

92 C6 glioma cells without altering TRAP-6 and carbachol Ca(2+) responses.

93 ivity-specifically, elevated Ca(2+) related (carbachol/Ca(2+) ionophore), but there was normal inhibi

94 ne microinjections of a cholinergic agonist, carbachol, can repeatedly elicit REM sleep-like episodes

95 The mixed muscarinic agonist carbachol (CAR) hyperpolarized all type II (A current) P

96 Here, we focus on the reaction of carbachol (carbamoylcholine) with AChE.

97 pressing M1 receptors, a muscarinic agonist (carbachol) causes a 40% decrease of F(surf) in normal me

98 ate (KA, 200 nm) and the cholinergic agonist carbachol (Cb, 10 mum) fast network oscillations, in the

99 hologic responses to the cholinergic agonist carbachol (Cch) and cholecystokinin (CCK-8), including 1

100 n increased maximal contractions (E(max)) to carbachol (CCh) and KCl.

101 nar cell responses to the muscarinic agonist carbachol (CCh) and the bile acid taurolithocholic acid

102 scarinic acetylcholine receptor, the agonist carbachol (Cch) caused strong activation of CFTR through

103 age clamped in the whole cell configuration, carbachol (CCh) evoked propagating Ca2+ waves which were

104 ulation; 3-4 muM L-glutamate (Glu) and 3 muM carbachol (CCh) evoked rapid Ca(2+) transients only in n

105 Importantly, the cholinergic agonist carbachol (CCh) induces gamma oscillations in vitro, via

106 ic fundus muscles stimulated by bath-applied carbachol (CCh) or cholinergic motor neurotransmission.

107 ter stimulation with the cholinergic agonist carbachol (Cch) or epidermal growth factor (EGF) for 5 m

108 The cholinergic agonist carbachol (Cch) stimulated the secretion of lacritin and

109 Carbachol (CCh) stimulation of HEK293 cells expressing w

110 epression), cholinergic agonist (5-10 microM carbachol (CCh)) reduced the amplitude of the first EPSP

111 We report that bath application of 3 mum carbachol (CCh), a muscarinic acetylcholine receptor ago

112 Carbachol (CCh), a muscarinic receptor-specific agonist,

113 muscarinic agonists oxotremorin-M (Oxo-M) or carbachol (CCh), although all three ligands have similar

114 Stimulation of isolated acinar cells with carbachol (CCh), histamine or ATP was associated with ma

115 Chronic application of the mAchR agonist, carbachol (Cch), induces Arc transcription via ERK signa

116 ined the contributions of Orai1 and TRPC1 to carbachol (CCh)-induced [Ca(2+)](i) signals and activati

117 hronic exposure to 10 mM histamine inhibited carbachol (CCh)-induced beta-hexosaminidase secretion an

118 he submucosal plexus) of rat proximal colon, carbachol (CCh)-induced Cl(-) secretion was decreased by

119 Carbachol (CCh)-mediated contraction was increased in bl

120 t on theta-frequency IPSC rhythms induced by carbachol (CCh).

121 ore stimulation with the cholinergic agonist carbachol (Cch, 10(-4) M) for 5 minutes.

122 Carbachol (CCh, 100 nm and 1 mum) induced a sustained in

123 Protein secretion was induced by lacritin or carbachol (Cch, positive control).

124 maintained during a progressive decrease of carbachol concentration, even down to concentrations tha

125 shortening during a progressive decrease of carbachol concentration.

126 Carbachol concentration/temporal-force responses were si

127 tion was strongly potentiated by low VIP and carbachol concentrations that individually were unable t

128 ibits the [Ca(2+)](i) signals induced by low carbachol concentrations, whilst those signals seen at h

129 Concentration/temporal responses to carbachol demonstrated similar sensitivities for bovine

130 The local photolysis of caged carbachol demonstrated that the functional expression of

131 Concentration/temporal responses to carbachol demonstrated tight coupling between force deve

132 ic receptor stimulation with the addition of carbachol, demonstrating "accentuated antagonism." Okada

133 The synchronizing action of carbachol depended on the glucose concentration used, su

134 treatment reversed these impairments whereas carbachol did not.

135 We also found that carbachol directly excited SLDsp neurons by activating a

136 reviously exposed to the cholinergic agonist carbachol, displayed longer neurites.

137 Furthermore, glucose and carbachol do not significantly affect Kv2.1 inactivation

138 toma cells, whereas the nonmitogenic agonist carbachol does not.

139 was possible to characterize the potency of carbachol (EC50=10.5 microM) and pirenzepine (IC50=4.2 m

140 The carbachol effect was blocked by atropine and SLM-driven

141 BIM I) produced the same enhancing effect on carbachol-evoked calcium mobilization as overexpressed D

142 th phorbol 12-myristate 13-acetate shortened carbachol-evoked calcium responses and occluded the effe

143 l) from patients with primary SS reduced the carbachol-evoked increase in [Ca2+]i in both mouse and h

144 -specific inactivation of ATG5 did not alter carbachol-evoked saliva and amylase secretion.

145 with nanosensors and their responsiveness to carbachol-evoked store release ( 400 nM).

146 timulated only with a Ca2+-mediated agonist (carbachol), exocytosis was followed by poor discharge as

147 soproterenol compared with controls, whereas carbachol failed to inhibit isoproterenol-stimulated NCX

148 Cells were also exposed to VIP, carbachol, forskolin, and/or 3-isobutyl-1-methylxanthine

149 n of TRPC1 protein by either thapsigargin or carbachol further protected SH-SY5Y cells from salsolino

150 In both exposed and control animals, 100 muM carbachol had a transient excitatory effect on spontaneo

151 proved DMTP, whereas the cholinergic agonist carbachol impaired performance at the highest dose teste

152 r (FLIPR) functional assay (EC50, 36 nM) and carbachol in a hippocampal slice electrophysiology assay

153 pendent Isc was also produced by basolateral carbachol in all preparations except rabbit and the H441

154 The effect of carbachol in astrocytes was due to the activation of M3

155 t promoted by the muscarinic receptor ligand carbachol in freshly dispersed rat parotid acinar cells.

156 receptor currents by the muscarinic agonist carbachol in hippocampal pyramidal cells.

157 cally exaggerated bradycardia in response to carbachol in mice and isolated perfused hearts and signi

158 agonist reverted the stimulatory effects of carbachol in naive mice to levels comparable with those

159 rmation stimulated by norepinephrine but not carbachol in transfected HEK293 cells.

160 skolin together is synergistic; both VIP and carbachol increase intracellular [Ca2+] in SLHMG cells;

161 Carbachol increased ATP release from lacrimal gland piec

162 Exposure of astrocytes to carbachol increased the expression of the extracellular

163 olinergic receptors with bath application of carbachol increased the firing rate of large (>20 mum di

164 captured; exposure to the muscarinic agonist carbachol increased the fluorescence to 220 +/- 74% (n =

165 Carbachol increased the phosphorylation of Pyk2 on tyros

166 Carbachol increased the probability of SR input to drive

167 As predicted from functional studies, carbachol increases F(surf) when cytoplasmic Ca(2) is in

168 stimulated by veratridine, but not by KCl or carbachol, indicating that the Ca2+ uniporter pathway pl

169 Fourth, carbachol induced a rapid and transient increase in endo

170 timulation of NO production by bradykinin or carbachol induced a significant reduction in MVO2 in wil

171 At the cellular level, carbachol induced an increase in the intracellular [Ca(2

172 The muscarinic agonist carbachol induced pronounced transient PKCbetaI transloc

173 istent with previous reports indicating that carbachol-induced [Ca(2+)](i) signals in these cells are

174 Ethanol caused a doubling in the carbachol-induced activation of the proteases trypsin an

175 e via Epac1 but is also involved in CCK- and carbachol-induced amylase release, with their action mos

176 nd that compound 6 is effective in reversing carbachol-induced contraction in the isolated strip prep

177 When rise of [Ca(2+)]pm was prevented, the carbachol-induced DAG and PKC responses were somewhat re

178 um responses in cortical neurons and affects carbachol-induced depletion of PIP2.

179 In mice with recurrent seizures, carbachol-induced enhancement of spontaneous IPSCs (sIPS

180 reduction of PTEN expression did not affect carbachol-induced externalization of TRPC6 but increased

181 e cellular and network mechanisms underlying carbachol-induced fast network oscillations in the hippo

182 Specifically, we show that carbachol-induced gamma oscillations (25-35 Hz) in rat h

183 ically identified CA1 and CA3 neurons during carbachol-induced gamma oscillations in mouse hippocampa

184 al potential measurements suggested that the carbachol-induced inward current was mediated mainly by

185 location of TRPC6 to the plasma membrane and carbachol-induced net Ca(2+) entry into T6.11 cells.

186 We found that carbachol-induced oscillations in rat CA3 have biphasic

187 0Hz range, and for the kainate-, but not the carbachol-induced oscillations, there was a small but si

188 re we compare the properties of kainate- and carbachol-induced oscillatory activity generated in CA3

189 Imatinib inhibited the carbachol-induced PCs of both juvenile and adult denuded

190 In contrast to WT, bradykinin- or carbachol-induced reduction in MVO2 was attenuated in nN

191 HHcy significantly decreased bradykinin- or carbachol-induced reduction of myocardial oxygen consump

192 ted salivary gland inflammation and enhanced carbachol-induced saliva secretion.

193 oligand binding and second messenger assays (carbachol-induced stimulation of phosphatidylinositol hy

194 by PIK-93, LY294002, or wortmannin decreased carbachol-induced translocation of TRPC6 to the plasma m

195 Whereas whole-cell carbachol-induced TRPC3 current was blocked by 3 microM

196 Carbachol-induced vasodilatation was increased in arteri

197 cting endothelin-induced vasoconstriction or carbachol-induced vasorelaxation.

198 n or selective thalamic activation caused by carbachol infusion in the VPM, the responses to AWs enha

199 Effects of carbachol infusion on patterns of neuronal activation du

200 Consistent with this idea, the ACh agonist carbachol inhibited presynaptic specialization of motorn

201 The carbachol-initiated phosphorylation of Ser(23) alpha1 su

202 xample, injection of the cholinergic agonist carbachol into the dorsomedial pons produces an REM slee

203 t direct infusion of the cholinergic agonist carbachol into the striatum, but not into the neighborin

204 ld refraction was measured before and during carbachol iontophoresis stimulated accommodation, a tota

205 his reaction are of special interest because carbachol is an isosteric analogue of the physiological

206 We found that carbachol is more effective at increasing REM sleep when

207 nd the arrestins also significantly enhanced carbachol-mediated activation of extracellular signal-re

208 in a significant decrease in thapsigargin or carbachol-mediated Ca(2+) influx.

209 GRK6, but not GRK5, significantly increased carbachol-mediated calcium mobilization.

210 2 or arrestin-3 also significantly increased carbachol-mediated calcium mobilization.

211 mM, but was decreased by 40 mM glucose, and carbachol-mediated dilation was unaffected.

212 Also, carbachol-mediated inhibition of NHE3 activity was aboli

213 showed that gadolinium-, thapsigargin-, and carbachol-mediated release of Ca(2+)(i) induced Shh expr

214 that modest doses of the cholinergic agonist carbachol normally decorrelate spontaneous activity gene

215 nsity) and endothelium-dependent dilatation (carbachol) of the MCA were not different between groups.

216 icantly augmented the stimulatory effects of carbachol on H508 cell proliferation and p90RSK activati

217 rts and significantly enhanced the effect of carbachol on inhibition of spontaneous action potential

218 aic acid eliminated the inhibitory effect of carbachol on isoproterenol-stimulated NCX current, indic

219 nd recorded pre- and postsynaptic effects of carbachol on SLDsp neurons.

220 ctin activity strongly reduced the effect of carbachol on the elongation of all the neurites, whereas

221 ied the general cholinergic receptor agonist carbachol onto neurons in dorsolateral PFC (DLPFC) of ma

222 ignificantly inhibited the ability of either carbachol or AC-42 to stimulate inositol phosphate accum

223 eptor or epidermal growth factor receptor by carbachol or epidermal growth factor stimulation induced

224 on currents activated by bath application of carbachol or intracellular infusion of GTPgammaS, demons

225 reduce GDNF secretion, while treatment with carbachol or long-term electrical stimulation enhances G

226 f the nicotinic agonist binding site by ACh, carbachol, or choline.

227 5' triphosphate (BzATP), cholinergic agonist carbachol, or the activator of conventional and novel PK

228 a1 was not blocked by PKC inhibitors, unlike carbachol- or phorbol 12-myristate 13-acetate-initiated

229 logical "two-concentration" acetylcholine or carbachol paradigm was developed and validated to determ

230 With increasing times during carbachol perfusion of glands, in situ, PKC-alpha redist

231 ield stimulation, as well as activation with carbachol, phenylephrine, and KCl, were lower in old tha

232 Interactions among carbachol, PKC inhibitors, phorbol 12-myristate 13-aceta

233 l stimulation, indicating that the siRNA and carbachol portions of the conjugate retained their funct

234 Consistent with this, carbachol potentiated GIP-mediated insulin release from

235 ive parotid cells isoproterenol enhanced the carbachol-promoted increases in [Ca(2+)](i) and oxygen c

236 e inhibitor ouabain reduced and enhanced the carbachol-promoted phosphorylation of Ser(23) and Ser(16

237 nduced sensitization of cholecystokinin- and carbachol-regulated Ca(2+) signaling in pancreatic acina

238 relaxed rapidly with comparable rates after carbachol removal and only 1.5-fold slower after KCl rem

239 orthosteric binding pocket caused a loss of carbachol response that could be rescued by BQCA.

240 nsient activation of muscarinic receptors by carbachol results in a long-lasting depression of synapt

241 Stimulation of M3R with carbachol significantly increased this association.

242 Carbachol stimulated the formation of disulfide bonds in

243 , stimulated with forskolin, stimulated with carbachol, stimulated with substance P, and, as a test f

244 This was associated with a reduction in carbachol-stimulated amylase release and an accumulation

245 also abrogates the ability of EGF to inhibit carbachol-stimulated basolateral K(+) currents.

246 re, we show that, in addition to suppressing carbachol-stimulated Ca(2+) release, Gbeta5-RGS7 enhance

247 g effects of ethanol on cholecystokinin- and carbachol-stimulated Ca(2+) signaling and intracellular

248 In the presence of this peptide, carbachol-stimulated calcium inhibition of NHE3 was lost

249 Carbachol-stimulated Cl(-) efflux and the protein levels

250 f extracellular Ca(2+), also reduced TG- and carbachol-stimulated ERK1/2 phosphorylation.

251 In contrast to mucus release, PGE(2)- and carbachol-stimulated fluid secretion was not dependent o

252 ist SCH-23390 (100 microM) did not alter the carbachol-stimulated glutamate release even though it in

253 ulline (10 microM) into the SN prolonged the carbachol-stimulated glutamate release in similar fashio

254 Carbachol-stimulated glutamate release was prolonged by

255 The P2X7 antagonist did not alter the carbachol-stimulated increase in [Ca2+]i or peroxidase.

256 n intestinal CaCC based on inhibition of ATP/carbachol-stimulated iodide influx in HT-29 cells after

257 eated cells, the inhibitory effect of EGF on carbachol-stimulated K(+) channel activity was lost.

258 Inhibition of PKC partially inhibited carbachol-stimulated MAPK activation while completely in

259 Chelation of Ca(2+) also partially inhibited carbachol-stimulated MAPK with no effect on phenylephrin

260 Prostaglandin E(2) (PGE(2))- and carbachol-stimulated mucus release was severely inhibite

261 e release by 60% and reduced CCK- as well as carbachol-stimulated pancreatic amylase release by 40%.

262 The c-src inhibitor PP1 inhibited carbachol-stimulated phosphorylation of Pyk2.

263 Inhibition of classical PKC proteins blocked carbachol-stimulated Ser(23) alpha1 subunit phosphorylat

264 Carbachol stimulation releases Gbetagamma subunits from

265 evation of intracellular calcium levels upon carbachol stimulation seen in these cells.

266 ide injection, the antinociceptive effect of carbachol stimulation was blocked.

267 of endocytosis at levels similar to those of carbachol stimulation, indicating that the siRNA and car

268 After carbachol stimulation, there was initially an anterior m

269 ity, irrespective of whether it is evoked by carbachol, store depletion, lanthanides or elevated intr

270 e opening rate for a subsaturating dosage of carbachol, suggesting that physostigmine does not intera

271 stinal peptide and/or forskolin but not with carbachol; synergy was absent in CF glands.

272 PCLS from Rgs5(-/-) mice contracted more to carbachol than those from WT mice, indicating that RGS5

273 r deactivation was significantly faster with carbachol than with acetylcholine and was significantly

274 imulation with concentrations of glucose and carbachol that accelerate hydrolysis of endogenous AA fr

275 ore stimulation with the cholinergic agonist carbachol, the alpha(1D)-adrenergic agonist phenylephrin

276 In the presence of the agonist carbachol, the effects of SLURP-1 on gene expression wer

277 -protein-coupled muscarinic receptor mimetic carbachol, the phorbol ester phorbol 12-myristate 13-ace

278 itions but after elevation of [Ca(2+)](i) by carbachol, this overlap was abolished.

279 hat they may contact different residues than carbachol to activate M(1) but occupy substantially over

280 The ability of pontine carbachol to elicit any cortical, hippocampal or brainst

281 Finally, by applying carbachol to increase EPSC activity, we observed that cl

282 further corroborated by the inefficiency of carbachol to increase IPSC frequency in these cells.

283 dB SPL, 4h) before and after application of carbachol to the DCN surface.

284 These constants for the binding of carbachol to the P-site are about an order of magnitude

285 Specifically, Ca(2+) entry seen after carbachol treatment in cells transiently expressing TRPC

286 rce generation during the first 2 mins after carbachol treatment), and myosin light chain phosphoryla

287 ifferences in sustained responses to KCl and carbachol treatments and washouts, respectively.

288 moderate differences in response to KCl and carbachol treatments, and relaxed rapidly with comparabl

289 The excitatory effect of carbachol was blocked by antagonists of M1 and M3 muscar

290 sphosphate production by cholecystokinin and carbachol was inefficient in Mist1-/- cells.

291 The cholinergic agonist carbachol was infused into the medial septum, and hippoc

292 Carbachol was synthesized with an active choline group a

293 ic acid, as well as to low concentrations of carbachol, was specifically dependent on protein kinase

294 muscarinic receptors, because the effects of carbachol were blocked by M1 receptor antagonists and lo

295 l NO synthase in response to the M3R agonist carbachol were diminished.

296 pressure elevation and IKACh sensitivity to carbachol were enhanced in Ex16 rats, implicating both c

297 ves in the presence of low concentrations of carbachol, which probably increased the tonic level of I

298 the synergistic combination of forskolin and carbachol, which produced near-maximal clearance rates r

299 initiated by the muscarinic receptor agonist carbachol, which promoted an increase to approximately 5

300 ependent FRET response for acetylcholine and carbachol with M(3)-AChR-N514Y.