ライフサイエンスコーパス: ACh

1 ACh also contributes to the use-dependent inhibition of

2 ACh also reduces glutamate release from mossy fibers by

3 ACh is a signaling molecule in the mammalian CNS, with w

4 ACh is an important modulator of breathing, including at

5 ACh is generated following mitochondrial production of a

6 ACh levels increased in viable heart tissue 10-14 d afte

7 ACh release from cholinergic axons is thus sufficient to

8 ACh stimulated the interaction of S100A4 with NM myosin

9 ACh stimulated the phosphorylation of NM myosin heavy ch

10 ACh, via M2 muscarinic receptors, contributes to the mod

11 ACh-evoked currents potentiated by the allosteric agonis

12 ACh-release is regulated in an autocrine manner.

13 ium-dependent vasodilator alone (Protocol 1: ACh or Protocol 2: low dose ATP); (ii) mild handgrip exe

14 3%; Middle Aged: 36 +/- 3%; Old: 15 +/- 2%; ACh: Young: 63 +/- 2%, Middle Aged: 34 +/- 3%; Old: 23 +

15 Acetylcholine (ACh) increased [Ca(2+) ]i with a time course similar to

16 Acetylcholine (ACh) is a potent neuromodulator capable of modifying pat

17 Acetylcholine (ACh) is the most important parasympathetic neurotransmit

18 Acetylcholine (ACh) plays an essential role in cortical information pro

19 ABSTRACT: Acetylcholine (ACh) released at the vertebrate nerve-muscle synapse is

20 ons between dopamine (DA) and acetylcholine (ACh) at striatal synapses.

21 nt neurotransmitters, such as acetylcholine (ACh).

22 for neurotransmitters such as acetylcholine (ACh).

23 is associated with attenuated acetylcholine (ACh) levels in prefrontal cortex.

24 nshaw cells by releasing both acetylcholine (ACh) and glutamate.

25 unction of neuromodulation by acetylcholine (ACh) and norepinephrine (NE) and afferent synaptic excit

26 holine receptors activated by acetylcholine (ACh) are brief.

27 hows that increasing cortical acetylcholine (ACh) levels alter specific aspects of the population cor

28 rotransmitter, T cell-derived acetylcholine (ACh) has recently been reported to play an important rol

29 ually modulated by endogenous acetylcholine (ACh).

30 sential biological sensor for acetylcholine (ACh) detection is constructed by immobilizing enzymes, a

31 ere we demonstrate a role for acetylcholine (ACh) in Drosophila.

32 s with normal or low glucose, acetylcholine (ACh), and/or mecamylamine.

33 We therefore investigated how acetylcholine (ACh), known to drive brain states of attention and arous

34 n was evaluated by inhibiting acetylcholine (ACh)-induced Pak activation through the expression of a

35 synaptic signal that inhibits acetylcholine (ACh) release at neuromuscular junctions.

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

37 e ability to directly measure acetylcholine (ACh) release is an essential step toward understanding i

38 ked by potassium (KCl 60 mM), acetylcholine (ACh 10 muM) or serotonin (5-HT 10 muM).

39 as shown that M(3) muscarinic acetylcholine (ACh) receptors (M3Rs) expressed by pancreatic beta cells

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

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

42 The neuromodulator acetylcholine (ACh) is crucial for several cognitive functions, such as

43 show that the neuromodulator acetylcholine (ACh) is essential to dlPFC working memory functions, but

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

45 ant efferent neurotransmitter acetylcholine (ACh) activates calyceal nicotinic ACh receptors (nAChRs)

46 e endogenous neurotransmitter acetylcholine (ACh) is known to affect the excitatory/inhibitory (E/I)

47 romeric alpha3beta4 nicotinic acetylcholine (ACh) receptors (nAChRs) are pentameric ligand-gated cati

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

49 demonstrate the secretion of acetylcholine (ACh) from BC upon stimulation with the Tas2R agonist den

50 nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes i

51 fast synaptic transmission of acetylcholine (ACh) in rodent medial prefrontal cortex (mPFC).

52 KEY POINTS: Phasic release of acetylcholine (ACh) in the neocortex facilitates attentional processes.

53 Phasic release of acetylcholine (ACh) in the neocortex facilitates attentional processes.

54 task relies on the release of acetylcholine (ACh) into the cortex from cholinergic neurons in the nuc

55 entiating the transmission of acetylcholine (ACh) via the cholinergic drug donepezil reduces the exte

56 erves are the main sources of acetylcholine (ACh) within the gastric mucosa.

57 ine, eliminated the effect of acetylcholine (ACh), but not of light, on isolated mouse sphincter musc

58 The rapid hydrolysis of acetylcholine (ACh), one of the key neurotransmitters in the human body

59 angiotensin II and a loss of acetylcholine (ACh)-mediated vasodilation.

60 ions (3 progressive doses) of acetylcholine (ACh; EDD) and sodium nitroprusside (endothelial-independ

61 preganglionic parasympathetic acetylcholine (ACh) neurons in the dorsal motor nucleus of the vagus (D

62 1: )) was shown to potentiate acetylcholine (ACh) in an M1 fluorometric imaging plate reader (FLIPR)

63 vation of CB2Rs by GW reduced acetylcholine (ACh)-, but not cholecystokinin (CCK)-induced Ca(2+) osci

64 es with elevation of striatal acetylcholine (ACh) levels.

65 al.SIGNIFICANCE STATEMENT The acetylcholine (ACh) arousal system in the brain is needed for robust at

66 in neuropathic pain rats, the acetylcholine (ACh)-dependent increase in neuronal excitability is redu

67 changes in the sensitivity to acetylcholine (ACh) and in the expression of key postsynaptic proteins.

68 duce, release, and respond to acetylcholine (ACh), but the functional role of cholinergic systems in

69 thod to quantify responses to acetylcholine (ACh): agonist sensitivity (EC50), maximal agonist-induce

70 brain states associated with acetylcholine (ACh) levels, such as attention and arousal and in pathol

71 While acute ACh application can modestly depolarize some Golgi cells

72 S100A4 depletion did not affect ACh-stimulated SM myosin regulatory light chain phosphor

73 ted with variable delay (up to 500 ms) after ACh application, but not by subthreshold depolarization

74 atation to the endothelium-dependent agonist ACh, whereas there was no change in the vasodilatory res

75 oncentration-response curve without altering ACh efficacy.

76 ibition, AChE limits the presence of ambient ACh and thus renders it unlikely that ACh influences tar

77 n (beta2alpha4)2alpha5 nAChRs also formed an ACh binding site.

78 helial proliferation and tumorigenesis in an ACh muscarinic receptor-3 (M3R)-dependent manner, in par

79 3%; Old + Adropin: 47 +/- 3%, P < 0.05) and ACh (Middle Aged + Adropin: 59 +/- 3%; Old + Adropin: 49

80 ssion and both flow (r = 0.81, P < 0.05) and ACh (r = 0.78, P < 0.05).

81 odulated differentially by endogenous DA and ACh in the shell, which may underlie the unique features

82 of ERG during coincident depolarization and ACh release leads to reduced late phase spike-frequency

83 tinic neurotransmission conveyed by GABA and ACh corelease, which inhibited DA neurons.

84 owing SD, Fos co-expression in Hcrt, HA, and ACh neurons (but not in 5HT neurons) was consistently el

85 Light and ACh share a common signaling pathway in sphincter muscle

86 tment with phenylephrine (PE) (10(-5) m) and ACh (10(-5) m).

87 in response to flow-induced shear stress and ACh.

88 ), indicative of impaired sympatholysis, and ACh or ATP infusion during mild exercise did not impact

89 As a demonstration of the method, we applied ACh or neostigmine in different spatial locations via th

90 Here we describe a method for applying ACh at different spatial locations within a single corti

91 s by which wake-on neurotransmitters such as ACh modulate RTN chemoreception, the results of the pres

92 Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expre

93 ential OAB urinary biomarkers including ATP, ACh, nitrite, MCP-1 and IL-5 and participants' confounde

94 ct as a PAM at M3Rs, significantly augmented ACh-induced insulin release from cultured beta cells and

95 timized the GRAB(ACh) (GPCR-activation-based ACh) sensor to achieve substantially improved sensitivit

96 eraction between this aromatic ring and both ACh and choline.

97 d largely on measures of extracellular brain ACh levels that require several minutes to generate a si

98 ctively, compared with currents activated by ACh alone, indicative of reduced calcium permeability.

99 V functions of alpha7 receptors activated by ACh when PAMs were bound to the allosteric binding site

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

101 Golgi cell hyperpolarization by ACh leads to a significant reduction in both tonic and e

102 t 50 mmHg, whereas vasodilatation induced by ACh (10(-5) m) was accompanied by a significant decrease

103 high ACh tone and disturbed significantly by ACh depletion.

104 erved when mouse myotubes were stimulated by ACh, with twitch duration and frequency most closely res

105 ntersubunit interface containing a canonical ACh binding site or to an alternative interface.

106 ow concentrations of acetylcholine chloride (ACh) and physostigmine, whereas the form containing two

107 In contrast, chronic ACh deprivation hindered whisker-evoked CBF responses an

108 Using this sensor, we revealed compartmental ACh signals in the olfactory center of transgenic flies

109 In contrast, ACh-mediated vasoconstriction was restored by expression

110 control ACh and ATP), indicative of impaired sympatholysis, and

111 electrochemical recordings measured cortical ACh following VS.

112 T-VIP neurons are a local source of cortical ACh that directly excite neurons throughout cortical lay

113 trated a reduced ability to support cortical ACh release in vivo compared with GTs after reverse-dial

114 ronic nicotine treatment (250 muM) decreased ACh-induced currents, and we found no additional effect

115 Indeed, VS decreased ACh release in the prefrontal cortex of male rats.

116 we show that the retrograde signal decreases ACh release by inhibiting the function of pre-synaptic U

117 ing control vasodilator infusions (DeltaFVC: ACh: -31 +/- 3 and ATP: -30 +/- 4%).

118 However, the role of lymphocyte-derived ACh in viral infection is unknown.

119 a probe of interocular dynamics to determine ACh's effects, via the acetylcholinesterase inhibitor (A

120 PEDOT modified FTO electrode for determining ACh level in serum samples, the applicability of biosens

121 o understand how these receptors distinguish ACh and Cho, we used single-channel electrophysiology to

122 bition on these neurons, reducing downstream ACh release to impair attention.

123 orylation is regulated by RhoA GTPase during ACh stimulation, and NM RLC phosphorylation is required

124 rteries, LECs depolarized (>15 mV) to either ACh or TRPV4 channel activation.

125 We found that acutely enhanced ACh tone significantly potentiated whisker-evoked CBF re

126 Lastly, peptidergic corelease enhances ACh-evoked responses in MBONs, suggesting an interaction

127 ion of VU6001221 attenuated potassium-evoked ACh levels in prefrontal cortex measured with in vivo mi

128 to levels observed during moderate exercise (ACh: -3 +/- 4; ATP: -18 +/- 4%).

129 et regions via slow changes in extracellular ACh concentrations.

130 This feedforward ACh-NGF axis activates the gastric cancer niche and offe

131 ent effects on Golgi cells and mossy fibers, ACh can either increase or decrease the spike probabilit

132 de approximately 50% more binding energy for ACh than for choline.

133 bited the highly potent catalytic enzyme for ACh, AChE, to facilitate measurement of ACh.

134 sor can be developed and detection limit for ACh is found to be 10nM.

135 Neither T-type VGCC isoform was required for ACh-induced inhibition of contraction, a mechanism by wh

136 finity and precise molecular specificity for ACh of its predecessor.

137 on behaviour distinctly from basal forebrain ACh inputs.

138 beta2 accessory subunits do not form ACh binding sites, but alpha4 accessory subunits do at t

139 week of running also induces switching from ACh to GABA expression in neurons in the caudal peduncul

140 ther that neurons utilizing serotonin, GABA, ACh, and short neuropeptide F interact in the LC12 optic

141 Here we optimized the GRAB(ACh) (GPCR-activation-based ACh) sensor to achieve subst

142 ed to estimate NVC, were enhanced under high ACh tone and disturbed significantly by ACh depletion.

143 These results illuminate how ACh strengthens higher cognition and help to explain why

144 ng in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and c

145 n) (carried by KCNQ4 channels), I(SK2) and I(ACh) (alpha9alpha10nAChRs) in OHCs and I(K,n) and I(K,f)

146 Our observations can be explained if ACh and glutamate are released from common vesicles onto

147 (-1) ; P < 0.05), whereas SNP did not impact ACh-mediated vasodilatation.

148 g the expression of HCN channels may improve ACh-DA reciprocity and motor function in Parkinson's dis

149 The results suggest that the difference in ACh versus Cho binding energies is determined by differe

150 Divergences in ACh and GABA levels may produce differential alterations

151 ch clamp data showing an age-related loss in ACh efficacy in evoking postsynaptic responses.

152 chieve substantially improved sensitivity in ACh detection, as well as reduced downstream coupling to

153 Increased ACh availability was assumed to accompany DA deficiency

154 Whereas acutely increased ACh enhanced neuronal responses and the resulting hemody

155 et effect of longer, optogenetically induced ACh release is to strongly hyperpolarize Golgi cells.

156 ant NM myosin S1943A in SM tissues inhibited ACh-induced endogenous NM myosin Ser1943 phosphorylation

157 nt, NM myosin S1943A, in SM tissues inhibits ACh-induced NM myosin filament assembly and SM contracti

158 ms resulted in increased GIRK currents ( I(K,ACh)) and a reduced inward rectification which was not c

159 fects on top of contractions induced by KCl, ACh and 5-HT.

160 Once liberated, ACh acts to trigger calcium release from the internal st

161 Local ACh application, or direct Kenyon cell activation, evoke

162 f these sites with MTSET reduced the maximal ACh evoked responses of these nAChRs by 30-50%.

163 rrent amplitude/cell capacitance) of 100 muM ACh-evoked currents.

164 celerated desensitization of 100 and 200 muM ACh-evoked currents.

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

166 ory neurons from mice lacking the muscarinic ACh type 1 receptor (M1R) exhibited enhanced neurite out

167 While the muscarinic ACh-receptors M3R and M1R are activating, M2R is inhibit

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

169 Here we find that a key neuromodulator, ACh, can alter the balance of excitation and inhibition

170 izing potentials in corticocallosal neurons, ACh generated prolonged mAChR-mediated depolarizing pote

171 ave a high affinity for the neurotransmitter ACh and a low affinity for its metabolic product choline

172 This increase is blocked by a nicotinic ACh receptor (nAChR) antagonist.

173 gh allosterically activated alpha7 nicotinic ACh receptor may affect intracellular calcium levels, su

174 uiring activation of glutamate and nicotinic ACh receptors.

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

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

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

178 ns demonstrated that neither low glucose nor ACh alone caused arrhythmias, but their combination indu

179 educed the exercise-induced amplification of ACh-mediated vasodilatation.

180 Such non-uniform application of ACh across the spatial extent of a cortical microcircuit

181 enuated the exercise-induced augmentation of ACh.

182 284 ( 1: ) also reduced the concentration of ACh required to inhibit [(3)H]N-methylscopolamine ([(3)H

183 ellent response to varying concentrations of ACh.

184 garotoxin and apamin, indicating coupling of ACh-mediated effects to small-conductance Ca(2+)-activat

185 onsible for the synthesis and degradation of ACh.

186 ll for the self-powered on site detection of ACh in plasma, which is based on the combination of an e

187 ms of receptor subtypes, and the dynamics of ACh hydrolysis.

188 actions underlying the beneficial effects of ACh on attention and working memory.

189 Paracrine effects of ACh released in response to denatonium included increase

190 n rat SOC, suggesting possible engagement of ACh-mediated modulation of neural activity in the MNTB.

191 ce (FVC) to local intra-arterial infusion of ACh (endothelium-dependent dilator) during resting condi

192 Infusion of ACh or ATP during mild exercise significantly attenuated

193 thelium-dependent signalling via infusion of ACh or ATP during moderate intensity exercise attenuated

194 he present study, intra-arterial infusion of ACh or ATP to augment endothelium-dependent signalling d

195 or moderate handgrip exercise + infusion of ACh or ATP to augment endothelium-dependent signalling.

196 ic neurons results in impaired inhibition of ACh release in the vSt and in anhedonic-like behavior.

197 out an increase in the area and intensity of ACh receptor labeling at the neuromuscular junction (NMJ

198 Moreover, many experimental manipulations of ACh have been done at a single spatial location, which i

199 for ACh, AChE, to facilitate measurement of ACh.

200 ACh and DA are reduced, the preponderance of ACh over DA contributes to the motor deficit.

201 are associated changes in the properties of ACh release during this period, we used a cochlear prepa

202 Although the production and release of ACh and DA are reduced, the preponderance of ACh over DA

203 That suggests that sympathetic co-release of ACh and NE may impair adaptation to high heart rates and

204 Flow-activated release of ACh from the endothelium is non-vesicular and occurs via

205 ys in which A1 neurons respond to release of ACh in challenging acoustic environments.

206 ain neurons may trigger increased release of ACh onto auditory neurons in primary auditory cortex (A1

207 in cholinergic neurons increasing release of ACh onto presynaptic and postsynaptic nAChRs in primary

208 inhibition in response to phasic release of ACh.

209 ed on the spatial and temporal resolution of ACh activity.

210 Here we investigate the role of ACh in regulating granule cell layer synaptic integratio

211 ponse relationship nor Zn(2+) sensitivity of ACh-evoked currents, suggesting that menthol does not ch

212 ), which catalyzes the rate-limiting step of ACh production, is robustly induced in both CD4(+) and C

213 (AChE) is fundamental for the termination of ACh impulse transmission.

214 CN) channels that encode the spike timing of ACh-releasing tonically active striatal interneurons (Ch

215 This differential transmission of ACh and GABA based on the postsynaptic target neuron is

216 cal new avenues to a better understanding of ACh in the brain.Dual Perspectives Companion Paper: Fore

217 that tone-evoked responses are dependent on ACh modulation by both nAChR subtypes.

218 ing that both antibodies bind at or near one ACh binding site at the alpha/gamma subunit interface.

219 eated with TSLP plus ACh, instead of TSLP or ACh alone.

220 ometry recording and two-photon imaging, our ACh sensor also enabled sensitive detection of single-tr

221 We have previously shown that at P9-P11, ACh release is supported by P/Q- and N-type voltage-gate

222 n of beta receptors, whereas parasympathetic ACh slows the heart through muscarinic receptors.

223 indicates that interaction with a particular ACh binding site is not the critical factor.

224 nt muscle via infusion of KCl amplified peak ACh-mediated vasodilatation (DeltaFVC saline: 97 +/- 15,

225 Exercise augmented peak ACh-mediated vasodilatation (DeltaFVC saline: 117 +/- 14

226 enhanced when DC were treated with TSLP plus ACh, instead of TSLP or ACh alone.

227 H-bonds position ACh and choline differently in the aromatic cage to gene

228 ne, or changes in pH, and three are putative ACh-gated cation channels.

229 and L-dopa-responsive DA deficiency reduces ACh availability and the transcription of hyperpolarizat

230 Electrical field stimulation releases ACh from nerves to increase RLC phosphorylation but not

231 he endothelium responds to flow by releasing ACh.

232 y responses that diminished after repetitive ACh application at RMPs were immediately rescued by pair

233 st time in comparison to previously reported ACh sensors.

234 zed by atropine, indicating that it requires ACh and muscarinic ACh receptor (mAChR) activation.

235 receptors are functional and exhibit robust ACh-gated currents blocked by alpha-bungarotoxin and str

236 k with single-site recordings or single-site ACh application should be interpreted with some caution,

237 In airway SM, ACh (acetylcholine) stimulated the binding of S100A4 to

238 Our results suggest that cell-specific ACh-mediated persistent firing in corticocollicular neur

239 The increase in striatal ACh relative to DA is heightened via D1-type DA receptor

240 increase in [Ca(2+)](i) in BC and subsequent ACh-release.

241 g at a single metabotropic receptor subtype, ACh exerts two opposing actions in cortical pyramidal ne

242 We conclude that ACh is not only a facilitator but also a prerequisite fo

243 We conclude that ACh is not only a potent modulator but also a requiremen

244 Together, these experiments demonstrate that ACh can modulate population-level granule cell responses

245 Functionally, we demonstrate that ACh contributes to sustaining high discharge rates and e

246 nergic fibers in rat neocortex and find that ACh enhances excitability by reducing Ether-a-go-go Rela

247 We find that ACh produces significant excitatory postsynaptic actions

248 Overall, we found that ACh in the OB increases glomerular sensitivity to odors

249 The current study found that ACh stimulation of nicotinic receptors comprised of alph

250 Our results support the hypothesis that ACh/NE modulation and afferent excitation define thalami

251 ensory-evoked NVC responses, indicating that ACh may alter the fidelity of hemodynamic signals in ass

252 Here, we provide the perspective that ACh, like most other neurotransmitters, exhibits both fa

253 ically stimulated zebrafish LL HCs show that ACh elicits a decrease in evoked Ca(2+) signals, regardl

254 Our results show that ACh released by motoneurons exerts a hitherto unknown fu

255 We show that ACh-release from BC via the bitter taste cascade leads t

256 These results suggest that ACh could play a key role in altering cerebellar learnin

257 tudy of the human visual system suggest that ACh is a likely component underlying interocular interac

258 Our observations suggest that ACh polarizes DC toward a Th2-promoting profile.

259 nucleus (RTN), where evidence suggests that ACh is essential for the maintenance of breathing.

260 mbient ACh and thus renders it unlikely that ACh influences target regions via slow changes in extrac

261 excitability is reduced dramatically and the ACh-induced persisting firing, which is critical for wor

262 ostly removed the light-induced, but not the ACh-triggered, increase in isolated sphincter muscle's t

263 onstructs demonstrated that a portion of the ACh binding domain, the E loop, is a key determinant.

264 CMPI produced a left shift of the ACh concentration-response curve without altering ACh ef

265 The improved version of the ACh sensor retains the subsecond response kinetics, phys

266 proach is that allosteric agents respect the ACh-dependent spatiotemporal control of M3R activity.

267 ([(3)H]NMS) binding to M1, left-shifting the ACh Ki approximately 19-fold at 10 muM.

268 h regions of subunits that contribute to the ACh binding site, whereas the lack of interface specific

269 olabeling of amino acids contributing to the ACh binding sites (alphaTyr(190),alphaTyr(198),gammaTrp(

270 We then systematically varied the ACh/NE and input levels to generate a complete map of th

271 can vary dramatically depending on where the ACh was applied.

272 wing cigarette smoking, altered neither the [ACh]-response relationship nor Zn(2+) sensitivity of ACh

273 50% less binding energy for Cho compared to ACh.

274 In contrast to ACh, exercise did not alter SNP-mediated vasodilatation

275 Ca(2+)-dependent BK K(+) channels coupled to ACh release at the MOC-OHC synapse and their shift in co

276 demonstrate a cellular mechanism, linked to ACh synthesis, that accounts for attenuated cholinergic

277 er, rescued SK responses were time-locked to ACh application, rather than to the timing of subsequent

278 d R188H mutants supported less relaxation to ACh, whereas relaxation mediated by the D40Y and R44H mu

279 y impact ways in which A1 neurons respond to ACh release.

280 adhesome signalling complexes in response to ACh, and inhibited actin polymerization and tension deve

281 ently amplified the vasodilatory response to ACh.

282 ereby inhibitory and excitatory responses to ACh in pyramidal neurons represent complementary mechani

283 tive reductions in postsynaptic responses to ACh.

284 ecific functional loss of nAChR signaling to ACh application in A1 layer 5.

285 onium (QA) and (2) AChRs respond strongly to ACh because an H-bond positions the QA to interact optim

286 Vasodilatation to ACh and vasoconstriction to phenylephrine (10(-9) to 10(

287 Taken together, ACh activation of nicotinic receptors via the vagus nerv

288 Traditionally, ACh distribution in cortex and associated changes in cor

289 olinergic transients and thus link transient ACh signaling with more sustained postsynaptic activity

290 the network of SACs differentially transmits ACh and GABA to DSGCs in a directional manner.

291 enabled sensitive detection of single-trial ACh dynamics in multiple brain regions in mice performin

292 n through L-type VGCCs contribute to trigger ACh release together with P/Q- and R-type VGCCs at P11-P

293 entities of the molecular players underlying ACh-mediated inhibition in the LL remain unknown.

294 inevitably results in spatially non-uniform ACh distribution.

295 n of the FA initiated on the arteriole using ACh microiontophoresis.

296 We therefore assessed the effects of varying ACh tone on whisker-evoked NVC responses in rat barrel c

297 n stellate sympathetic neurons and vesicular ACh transporter immunoreactivity in tyrosine hydroxylase

298 Here, we analyzed whether ACh could also modulate the functional profile of DC.

299 Treatment of DC with ACh stimulated the expression of the Th2-promoter OX40L,

300 Stimulation with ACh caused NM myosin filament assembly, as assessed by a