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 and FSK stimulated VASP Ser(157) phosphorylation by

3 ACh has long been considered important for the CO2/H(+)-

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 depolarized VIP BCs whereas PV BCs depolariz

8 ACh stimulated the phosphorylation of NM myosin heavy ch

9 I inhibited ( approximately 35% at 10microM) ACh responses of (alpha4)2(beta2)3nAChRs and fully inhib

10 responses of (alpha4)3(beta2)2nAChR to 10muM ACh (EC10) by 400% and with anEC50of approximately 1micr

11 Acetylcholine (ACh) can elicit striatal DA release through activation o

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

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

14 Acetylcholine (ACh) is crucial for cognitive functions.

15 Acetylcholine (ACh) is the most important parasympathetic neurotransmit

16 Acetylcholine (ACh) is thought to facilitate cortical plasticity during

17 Acetylcholine (ACh) released at the vertebrate nerve-muscle synapse is

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

19 with the contractile agonist acetylcholine (ACh) or the adenylyl cyclase activator, forskolin (FSK),

20 potency of the full agonists, acetylcholine (ACh), carbachol, and oxotremorine-M, while significantly

21 le of norepinephrine (NE) and acetylcholine (ACh) triggering opposing actions.

22 sed sensitivity to low pH and acetylcholine (ACh), which caused inappropriate Ca(2+) release and prem

23 nt neurotransmitters, such as acetylcholine (ACh).

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

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

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

27 inhibited currents evoked by acetylcholine (ACh) at rat alpha3beta2 (IC50 = 10.7 nM), whereas a 70-f

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

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

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

31 units are involved in forming acetylcholine (ACh) binding sites at their interfaces.

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

33 The enzyme, AChE hydrolyzes acetylcholine (ACh) to choline (Ch) which in turn interacts with AuQC@B

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 -46, a member of the Cys-loop acetylcholine (ACh)-gated chloride (ACC) channel family, localizes to p

38 ating the heart begin to make acetylcholine (ACh), which slows heart rate and decreases contractility

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

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

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

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

43 Neuromuscular acetylcholine (ACh) receptors have a high affinity for the neurotransmi

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 zyme for the neurotransmitter acetylcholine (ACh).

47 rotective agent and nicotinic acetylcholine (ACh) receptors (nAChRs) as targets for neuroprotection,

48 odulators (PAMs) of nicotinic acetylcholine (ACh) receptors (nAChRs) have potential clinical applicat

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

50 both muscarinic and nicotinic acetylcholine (ACh) receptors.

51 he role of co-transmission of acetylcholine (ACh) and GABA from starburst amacrine cells (SACs) to di

52 used to record the release of acetylcholine (ACh) by neuronal tissue cultivated on the gate area upon

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

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

55 tive fluorescent detection of acetylcholine (ACh) using bovine serum albumin (BSA) protected atomical

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 d with the putative action of acetylcholine (ACh), GABA and monoamines, which lead to transitions bet

59 ity, characterized by loss of acetylcholine (ACh), is one of the hallmarks of Alzheimer's disease (AD

60 erase-catalyzed hydrolysis of acetylcholine (ACh).

61 1: )) was shown to potentiate acetylcholine (ACh) in an M1 fluorometric imaging plate reader (FLIPR)

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

63 Optogenetically released acetylcholine (ACh) from medial septal afferents activates muscarinic r

64 hydrolysis of newly released acetylcholine (ACh), in the cortex of animals reporting the presence of

65 tudies have demonstrated that acetylcholine (ACh) alters the frequency response areas of auditory neu

66 We find that acetylcholine (ACh) is the most broadly used neurotransmitter and we an

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

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

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

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

71 helium-dependent vasodilators acetylcholine (ACh) and adenosine triphosphate (ATP), the endothelium-i

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

73 tamine; HA), basal forebrain (acetylcholine; ACh), dorsal raphe (serotonin; 5HT), and singly labeled

74 A third low affinity ACh binding site is formed when this accessory subunit i

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

76 oncentration-response curve without altering ACh efficacy.

77 expression of choline acetyltransferase, an ACh synthase, was reduced and extracellular ACh levels w

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

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

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

81 pha6, and beta3 nAChR subunit expression and ACh-evoked currents.

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

83 uggest monosynaptic release of both GABA and ACh.

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 o experiments examining the effect of NE and ACh on rabbit cardiac action potential duration revealed

88 tation versus familiar taste recognition and ACh levels were associated with the propensity to acquir

89 phaG153) affect GABA activation similarly as ACh activation, whereas a mutation at the complementary

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

91 Furthermore, the interaction between ACh dip and DA peak, via D1R and M4R, is synergistic.

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

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

94 re the regulation of AOB and MOB circuits by ACh, and how cholinergic modulation influences olfactory

95 n SVs prepared from the IPN was increased by ACh, indicating vesicular synergy.

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

97 nisms clearly differ from those initiated by ACh, but much remains undefined.

98 y type neurons with a M-current regulated by ACh.

99 high ACh tone and disturbed significantly by ACh depletion.

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

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

102 d the infarction-induced increase in cardiac ACh.

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

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

105 antagonism had opposite effects on cortical ACh levels in novel taste presentation versus familiar t

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

107 Previous work has suggested that decreased ACh activity in AD may contribute to pathological change

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

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

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

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

112 dothelium-dependent hyperpolarization (EDH), ACh trials were repeated with combined nitric oxide synt

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

114 evidence that activation of CB2Rs eliminates ACh-induced Ca(2+) oscillations and L-arginine-induced e

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

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

117 receptor (CKR-2) potentiate tonic and evoked ACh release at Caenorhabditis elegans neuromuscular junc

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

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

120 p exercise; and (3) combined mild exercise + ACh, ATP, SNP, or KCl infusions in healthy adults.

121 ACh synthase, was reduced and extracellular ACh levels were significantly reduced in DD mice.

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

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

124 to ATP citrate lyase (ACL), a key enzyme for ACh synthesis, and transports it toward neurite terminal

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

126 R5-R20, X5, Fres, ALX after provocations for ACh or Hist in all patients with asthma, but not in pati

127 At the same time, the genes required for ACh synthesis increased in stellate ganglia, which conta

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

129 a5/alpha4 and beta3/alpha4 interfaces formed ACh binding sites in (alpha4beta2)2alpha5 and (alpha4bet

130 essory subunits and not take part in forming ACh binding sites.

131 Furthermore, ACh influenced the input-output relationship of mitral c

132 timated the spatiotemporal profiles of GABA, ACh, and glutamate receptor-mediated synaptic activity i

133 GABA/ACh corelease may have major implications for modulation

134 low affinity to the ACh binding sites ([(3)H]ACh, IC50 = 1 mM).

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

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

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

138 A further decrease in ACh leads to a high degree of synchrony within traveling

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

140 Divergences in ACh and GABA levels may produce differential alterations

141 sumption, there is a significant increase in ACh release in the insular cortex (IC), a highly relevan

142 th some studies showing they are involved in ACh-dependent EEG desynchronization, and others suggesti

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

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

145 effectively reversed the effect of increased ACh signaling in a mouse model of depression.

146 toreceptors on cholinergic terminals inhibit ACh release and subsequent nAChR-dependent DA release.

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

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

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

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

151 action of GRK2 with the M3-acetylcholine (M3-ACh) receptor as well as Gq-protein subunits with high s

152 nces the extent and stability of the GRK2-M3-ACh receptor interaction, and that not only Gbetagamma b

153 transmitters seen in fish (5HT) and mammals (ACh and adenosine).

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

155 phenoxybenzamine, as it reduced the maximal ACh response.

156 84 bound to M1 mAChR in the presence of 1 mM ACh with Kd, 4.23 nM, and saturable binding capacity (Bm

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

158 iated depolarizing potentials and muscarinic ACh receptor (mAChR)-mediated hyperpolarizing potentials

159 ver, it remains controversial how muscarinic ACh receptors (mAChRs) modulate striatal DA release, wit

160 conserved circuit, activation of muscarinic ACh receptors revealed marked differences in cholinergic

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

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

163 se from the autocrine action of non-neuronal ACh released by the endothelium.

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

165 In corticocollicular neurons, ACh release also generated nAChR-mediated depolarizing p

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

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

168 old higher affinity for the neurotransmitter ACh.

169 presses Cl(-) secretion induced by nicotinic ACh receptor activation via a Gi/o pathway.

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

171 lices, we found that ACh generated nicotinic ACh receptor (nAChR)-mediated depolarizing potentials an

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

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

174 l DA release through activation of nicotinic ACh receptors (nAChRs) on DA axonal projections.

175 Furthermore, reducing nicotinic ACh receptor subunit expression in MBONs compromises odo

176 vivo pharmacology, we find that increased OB ACh leads to dynamic, activity-dependent bi-directional

177 h a thioreactive reagent blocked activity of ACh and NS9283 at the accessory site.

178 An expression pattern analysis of ACh-gated anion channels furthermore suggests that ACh m

179 ddress how microiontophoretic application of ACh modulates SSA in the IC of the anesthetized rat.

180 monstrate that the increased availability of ACh exerts transient functional changes in partially ada

181 284 ( 1: ) also reduced the concentration of ACh required to inhibit [(3)H]N-methylscopolamine ([(3)H

182 was determined at various concentrations of ACh and AChE.

183 ellent response to varying concentrations of ACh.

184 onsible for the synthesis and degradation of ACh.

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

186 /tufted cells, we investigated the effect of ACh on the glomerular responses to increasing odor conce

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

188 logical tools to characterize the effects of ACh on baseline activity and CO2/H(+)-sensitivity of RTN

189 However, the effects of ACh on OB glomerular odor responses remain unknown.

190 The effects of ACh on RTN chemoreceptor activity were also blunted by i

191 Therefore, elucidation of the effects of ACh on the excitability of corticocollicular neurons wil

192 n relearning, we investigated the effects of ACh release on both L5B corticocallosal and corticocolli

193 cent monitoring AChE-catalyzed hydrolysis of ACh is possible through the H-function properties of Tb(

194 he real time monitoring of the hydrolysis of ACh using electrospray ionization mass spectrometry (ESI

195 Infusion of ACh or ATP during mild exercise significantly attenuated

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

197 We also show that the level of ACh determines how sensitive network activity is to syna

198 by the differences in the relative level of ACh.

199 to a type 1 PRC observed in the presence of ACh.

200 P-H is essential for the local production of ACh for morphogenesis and neurotransmission.

201 he cell-specific and cognitive properties of ACh.

202 Regulation of ACh level can account for dynamical changes between func

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

204 e possibility that sympathetic co-release of ACh and NE may impair adaptation to high heart rates and

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

206 inhibition in response to phasic release of ACh.

207 that PEA selectively affected the rundown of ACh currents in epsilon-AChRs.

208 ase (ChAT), leading to enhanced secretion of ACh.

209 e insights into the role and significance of ACh in determining patterns of cortical activity and fun

210 , although the physiological significance of ACh-induced activation of the endothelium is unknown.

211 athetic nerves that are the normal source of ACh in the heart.

212 nes of evidence confirmed that the source of ACh was sympathetic nerves rather than parasympathetic n

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

214 In contrast, ML380 enhanced only ACh potency after receptor alkylation, with no effect on

215 necessary for the activation of Hcrt, HA, or ACh wake-active neurons, which may underlie the milder c

216 ated by STIM1 in response to thapsigargin or ACh.

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

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

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

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

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

222 rdiac sympathetic nerves transiently produce ACh after myocardial infarction (MI).

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

224 lpha3)3(beta4)2 nAChRs to ACh while reducing ACh-induced whole-cell currents.

225 We further show that endogenously released ACh can modulate Up/Down states through the activation o

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

227 ical field stimulation (EFS), which releases ACh from nerves, increased force and RLC phosphorylation

228 he endothelium responds to flow by releasing ACh.

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

230 st time in comparison to previously reported ACh sensors.

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

232 Thus, we show ACh is an autocrine signalling molecule released from en

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

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

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

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

237 We find that ACh produces significant excitatory postsynaptic actions

238 We found that ACh activates RTN chemoreceptors in a dose-dependent man

239 enetics in mouse brain slices, we found that ACh generated nicotinic ACh receptor (nAChR)-mediated de

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

241 We found that ACh initiates responses to motion in natural scenes or u

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

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

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

245 nt study, we show at the cellular level that ACh increases RTN chemoreceptor activity by a CO2/H(+) i

246 We propose that ACh-mediated persistent firing in corticocollicular neur

247 diac action potential duration revealed that ACh blunted both the NE-stimulated decrease in cardiac a

248 These results show that ACh activates RTN chemoreceptors by a CO2/H(+) independe

249 or without ACh to ex vivo hearts showed that ACh partially reversed the NE-stimulated decrease in car

250 uired for RTN chemoreception by showing that ACh, similar to serotonin and other modulators, controls

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

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

253 ted anion channels furthermore suggests that ACh may also operate very broadly as an inhibitory neuro

254 reporting the presence of cues suggests that ACh may have a more specialized role in cognitive proces

255 These results dispel the theory that ACh is required for RTN chemoreception by showing that A

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

257 Kenyon cells express the ACh-processing proteins ChAT and VAChT, and reducing the

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

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

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

261 or the alpha4/beta2 site) did not act on the ACh sites formed by the alpha5/alpha4 or beta3/alpha4 in

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

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

264 it bound with only very low affinity to the ACh binding sites ([(3)H]ACh, IC50 = 1 mM).

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

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

267 The firing response of RTN chemoreceptors to ACh was mimicked by a muscarinic receptor agonist (oxotr

268 50% less binding energy for Cho compared to ACh.

269 ly 15% in Young MAs while all dilatations to ACh were abolished.

270 n Young but not Old MAs while dilatations to ACh were not different between age groups.

271 oung MAs while abolishing all dilatations to ACh.

272 normalized bronchial hyperresponsiveness to ACh or Hist.

273 normalized bronchial hyperresponsiveness to ACh or Hist.

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

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

276 e sensitivity of (alpha3)3(beta4)2 nAChRs to ACh while reducing ACh-induced whole-cell currents.

277 opmental transition from production of NE to ACh and we provide evidence that mouse cardiac sympathet

278 olymerization and contraction in response to ACh, but it did not affect myosin light chain phosphoryl

279 olymerization and contraction in response to ACh.

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

281 The endothelium is exquisitely sensitive to ACh, although the physiological significance of ACh-indu

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

283 Potentiation of tonic ACh release persists in mutants deficient for egl-30 Gal

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

285 meric alpha4beta2* nAChRs typically have two ACh binding sites at alpha4/beta2 interfaces and a fifth

286 mporal resolution are critical to understand ACh neuromodulation.

287 Nicotine also upregulated ACh-induced currents in DA neurons by approximately 2.5-

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

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

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

291 protein gene product (PGP)9.5, the vesicular ACh transporter, and the high-affinity choline transport

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

293 s to dissect the signalling pathway by which ACh activates these neurons.

294 r circuits or the specific neurons via which ACh exerts its cognitive effects remain unknown, it is k

295 r circuits or the specific neurons via which ACh exerts its cognitive effects remain unknown, it is k

296 esults provide synaptic mechanisms via which ACh may mediate its effects on AC receptive fields.

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

298 cent decrease in FEV1 after provocation with ACh or Hist.

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

300 Global application of NE with or without ACh to ex vivo hearts showed that ACh partially reversed