ライフサイエンスコーパス: A1 receptor

1 ed by PD81723, an allosteric enhancer of the A1 receptor.

2 y DPCPX, indicating a prominent role for the A1 receptor.

3 ow are mediated by adenosine but not via the A1 receptor.

4 uld be ameliorated by blocking the adenosine A1 receptor.

5 n of the A2A receptor on the neuroprotective A1 receptor.

6 that produced by activation of the adenosine A1 receptor.

7 y formed adenosine can chaperone its cognate A1 receptor.

8 ffinity indistinguishable from the wild-type A1 receptor.

9 indings were recapitulated for the wild-type A1 receptor.

10 tonically inhibited by adenosine acting via A1 receptors.

11 siently be provoked after blocking adenosine A1 receptors.

12 , metabotropic glutamate mGlu5 and adenosine A1 receptors.

13 ells showed enhanced responses to M2 but not A1 receptors.

14 rescued presynaptic inhibition by adenosine A1 receptors.

15 vealed greater A2B selectivity over A2A than A1 receptors.

16 adenosine (CPA) it appears to be mediated by A1 receptors.

17 thanol is mediated through myocyte adenosine A1 receptors.

18 y C fibre terminals through an activation of A1 receptors.

19 appears to be due to activation of adenosine A1 receptors.

20 stimulate PRL release in vitro by activating A1 receptors.

21 hypoxia induces dilatation only by acting on A1 receptors.

22 nglia, probably by activation of presynaptic A1 receptors.

23 tion of cAMP formation through activation of A1 receptors.

24 nd/or A2B but excluding the participation of A1 receptors.

25 A binding could be attributed to labeling of A1 receptors.

26 tion through activation of central adenosine A1 receptors.

27 amidal neurons via activation of presynaptic A1 receptors.

28 ogeneous activation of presynaptic adenosine A1 receptors.

29 ulsant acting on excitatory synapses through A1 receptors.

30 ive consequences through a pathway involving A1 receptors.

31 ciency was significantly reduced by blocking A1-receptors.

32 dent on adenosine-induced PKC activation via A1-receptors.

33 ateral RA had significantly higher adenosine A1 receptor (2.7+/-1.7-fold; P<0.01) and GIRK4 (1.7+/-0.

34 , Ki=7 nM) and selectivity for the adenosine A1 receptor (915-fold versus adenosine A2A receptor; 12-

35 Adenosine A1 receptor (A1-AdoR) function in rat ventricles has pre

36 retic action of a highly selective adenosine A1 receptor (A1AdoR) antagonist, 1,3-dipropyl-8-[2-(5,6-

37 esis that a partial agonist of the adenosine A1 receptor (A1AdoR) may cause a greater attenuation of

38 is study, we targeted the cochlear adenosine A1 receptor (A1AR) by trans-tympanic injections of the a

39 In this study, we show that the adenosine A1 receptor (A1AR) protects against cisplatin ototoxicit

40 Adenosine A1 receptor (A1AR) subtype present on renal proximal tub

41 Allosteric modulation of adenosine A1 receptors (A1ARs) offers a novel therapeutic approach

42 -term depression (LTD) mediated by adenosine A1 receptor (A1R) activation at corticostriatal synapses

43 of A1 receptor signaling using an adenosine A1 receptor (A1R) antagonist, 8-cyclopentyl-1,3-dimethyl

44 cortical actin polymerization via adenosine A1 receptor (A1R) induction of a Rho GTPase CDC42-depend

45 The adenosine A1 receptor (A1R) is a key mediator of the neuroprotecti

46 activity through activation of the adenosine A1 receptor (A1R), resulting in antinociception and high

47 synapses resulting in an enhanced adenosine A1 receptor (A1R)-dependent protective tone despite lowe

48 ate adenosine concentration and/or adenosine A1 receptors (A1R) in the brain.

49 s a neuromodulator acting through inhibitory A1 receptors (A1Rs) and facilitatory A2ARs, which have s

50 The suppression was mediated by presynaptic A1 receptors (A1Rs) because it was blocked by a selectiv

51 Activation of presynaptic adenosine A1 receptors (A1Rs) causes substantial synaptic depressi

52 Adenosine A1 receptors (A1Rs) in human and rodent brains can be vi

53 Because very little is known about adenosine A1 receptors (A1Rs) in the spinal cord, we determined th

54 hippocampal neurons, activation of adenosine A1 receptors (A1Rs) or GABA(B) receptors on synaptic ter

55 n mice by increasing activation of adenosine A1 receptors (A1Rs).

56 rosynaptic plasticity; blockade of adenosine A1 receptors abolished it.

57 rosynaptic plasticity: blockade of adenosine A1 receptors abolished weight dependence, while increase

58 Adenosine A1 receptor activation also impaired the expression of b

59 fect of acupuncture is mediated by adenosine A1 receptor activation at the acupuncture point, we here

60 The inhibitory modulation of adenosine A1 receptor activation by hydroxylamine suggests the pre

61 Adenosine A1 receptor activation depresses excitatory transmission

62 Adenosine A1 receptor activation dose-dependently and selectively

63 However, endogenous A1 receptor activation during cortical seizures in vivo

64 Given the central role demonstrated for A1 receptor activation in determining synaptic amplitude

65 d excitatory neurotransmission via adenosine A1 receptor activation in spinal cord slices from wild-t

66 of trigeminovascular nociception, adenosine A1 receptor activation leads to neuronal inhibition with

67 nal efficacy and therefore the heterogeneous A1 receptor activation seen in the mature neocortex appe

68 echanical allodynia via peripheral adenosine A1 receptor activation.

69 Adenosine elicits cardioprotection through A1-receptor activation.

70 mical property of dipole and selects against A1 receptor activity, generated a correlated final model

71 we report a novel dual role of the adenosine A1 receptor (Adora1) as an E2/ERalpha target and a regul

72 potential glucagon inhibitor, the adenosine A1 receptor (Adora1), is gradually diminished in alpha-c

73 e thought to require activation of adenosine A1 receptors (adorA1Rs) and release of transmitter molec

74 The selective A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CC

75 te receptor antagonist MK-801; the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CC

76 The A1 receptor agonist 2-Chloro-N6-cyclopentyladenosine (CC

77 However, the A1 receptor agonist 2-Chloro-N6-cyclopentyladenosine and

78 stantial increase in CoRCF and CoVC, but the A1 receptor agonist 2-chloro-N6-cyclopentyladenosine had

79 ) receptor agonist baclofen or the adenosine A1 receptor agonist 2-chloroadenosine, short-term synapt

80 These data are consistent with adenosine A1 receptor agonist actions on REM sleep mediated throug

81 or sodium nitroprusside (SNP), the adenosine A1 receptor agonist CCPA (2-chloro-N6-cyclopentyladenosi

82 rats were treated IT with the selective Ado A1 receptor agonist cyclohexyladenosine (CHA) or vehicle

83 Intrastriatal microinfusion of adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA) and ant

84 cholinergic neurons, the selective adenosine A1 receptor agonist N6-cyclohexyladenosine, administered

85 was mimicked by perfusion with the adenosine A1 receptor agonist N6-cyclopentyladenosine and prevente

86 Microinjection of adenosine A1 receptor agonist or an inhibitor of adenylyl cyclase

87 Adenosine and the A1 receptor agonist R-phenylisopropyl adenosine (RPIA) r

88 Similarly neither the A1 receptor agonist R-phenylisopropyladenosine (R-PIA),

89 Direct injection of an adenosine A1 receptor agonist replicated the analgesic effect of a

90 cked by exogenous adenosine or the selective A1 receptor agonist, 2-chloro-N6-cyclopentyl adenosine.

91 lices containing the PnOc incubated with the A1 receptor agonist, cyclohexaladenosine (10(-8) M).

92 The selective low efficacy adenosine A1 receptor agonist, GR190178 (30-1000 microg/kg i.v.),

93 nistration of the highly selective adenosine A1 receptor agonist, GR79236 (3-100 microg/kg) had a dos

94 ialanate, a first-in-class partial adenosine A1 receptor agonist, has the potential to improve severa

95 N6-Cyclopentyl adenosine (adenosine A1 receptor agonist, Kd = 1 nmol/l) did not affect GLUT1

96 ystemic injection of the selective adenosine A1 receptor agonist, N(6)-cyclohexyladenosine (CHA; 0.3

97 In Experiment 1, the selective adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA), or s

98 ould be demonstrated only with the selective A1-receptor agonist 2-chloro-N6-cyclopentyladenosine and

99 denosine (CGS-21680; 100 nM), but not by the A1-receptor agonist N6-cyclopentyladenosine (CPA).

100 5.5% with SfA; P<0.001), CCPA (the adenosine A1-receptor agonist, 200 nmol/L) (24.9+/-4.5% versus 54.

101 cement of [3H]DPCPX binding by the selective A1-receptor agonist, N6-p-sulfophenyladenosine (SPA), yi

102 ts of capadenoson (CAP), a partial adenosine A1-receptor agonist, on left ventricular (LV) function a

103 The selective adenosine A1 receptor agonists 2-chloro-N6-cyclopentyladenosine (C

104 Intrathalamic infusion of A1 receptor agonists directly reduces tremor, whereas ad

105 derable literature to suggest that adenosine A1 receptor agonists may have anti-nociceptive effects,

106 tric oxide synthase inhibitors and adenosine A1 receptor agonists.

107 lts support development of partial adenosine A1-receptor agonists for the treatment of chronic heart

108 Therapy with adenosine A1-receptor agonists, however, is limited by undesirable

109 distributions that spanned those of both the A1 receptor agonized and antagonized conditions.

110 Overexpressing the adenosine A1 receptor also led to increased protection against isc

111 Blockade of A1 receptors ameliorated the depression caused by adenos

112 Allosteric enhancers of the adenosine A1 receptor amplify signaling by orthosteric agonists.

113 eceptor, dopamine transporter, and adenosine A1 receptor and decreased adenosine A2A receptor express

114 ion was blocked in the presence of adenosine A1 receptor and GABAB receptor blockade.

115 were combined with homology modeling of the A1 receptor and in silico screening of an allosteric enh

116 A areas with highest expression of adenosine A1 receptor and its downstream GIRK (G protein-coupled i

117 (R)-phenylisopropyl]adenosine from rat brain A1 receptors and [3H]2-[p-(2-carboxyethyl)phenyl-ethylam

118 ments using [3H]cyclohexyladenosine to label A1 receptors and [3H]CGS 21680 to label A2A receptors.

119 M, respectively, at the rat and cloned human A1-receptors and with 1800-fold (rat) and 2400-fold (hum

120 which was prevented by blockade of adenosine A1 receptors, and decreased expression of genes involved

121 racellular Ado, activation of inhibitory Ado A1 receptors, and decreased seizure generation, the desi

122 at is mediated mainly by adenosine acting on A1 receptors, and that the vasoconstrictor effects of sy

123 itive potassium (K(ATP)) channels, adenosine A1 receptors, and the effects of different levels of hal

124 ilocapnic HVR; (2) these impairments require A1 receptors; and (3) SF of OSA may exacerbate OSA via i

125 tor than in those cells expressing the human A1 receptor (ANOVA and posttest comparison, P<0.01).

126 Moreover, adenosine A1 receptor antagonism had larger effects on theta respo

127 ac arrhythmias and seizures due to adenosine A1-receptor antagonism.

128 xogenous adenosine, or a selective adenosine A1 receptor antagonist (8-cyclopentyl-1, 3-dimethylxanth

129 The adenosine A1 receptor antagonist 1,3-dipopylcyclopentylxanthine pr

130 0.9%) by systemic injection of the adenosine A1 receptor antagonist 8-CPT (2.5 mg kg(-1)) approximate

131 ly reversed in the presence of the adenosine A1 receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthi

132 Both the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

133 ibitor l-NAME (Group 1, n = 8) and adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

134 The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

135 s a mediator of IPC, the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

136 The concomitant presence of the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

137 The selective A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

138 The selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin

139 the administration of a selective adenosine A1 receptor antagonist but not by a selective adenosine

140 Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhi

141 or administration of the selective adenosine A1 receptor antagonist dipropylcyclopentylxanthine (DPCP

142 arge induced by adenosine was blocked by the A1 receptor antagonist DPCPX (10 microM) but remained un

143 ould be inhibited by the selective adenosine A1 receptor antagonist DPCPX (300 microg/kg; P < 0.05).

144 fter administration of a selective adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropyl

145 .4 nM for antagonism of CPA by the adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropyl

146 The adenosine A1 receptor antagonist DPCPX did not affect the resting

147 N6-cyclopentyladenosine and prevented by the A1 receptor antagonist N-0861.

148 acerebroventricular infusion of an adenosine A1 receptor antagonist produced a similar decrease in se

149 Here, we show that the adenosine A1 receptor antagonist rolofylline (KW-3902) is alleviat

150 Randomized Study of the Selective Adenosine A1 Receptor Antagonist Rolofylline for Patients Hospital

151 ble to that of BG9928, a selective adenosine A1 receptor antagonist that is currently in clinical tri

152 ropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist that is permeable to the blood br

153 Imidazoline 14 is a competitive adenosine A1 receptor antagonist with a pA2 value of 8.88 and is h

154 (4H)-one, is a particularly potent adenosine A1 receptor antagonist with good selectivity over the ot

155 In the search for a selective adenosine A1 receptor antagonist with greater aqueous solubility t

156 of SPWs in slices treated with an adenosine A1 receptor antagonist, a finding that links the present

157 y 1,3-dipropyl-8-cyclopentylxanthine, an Ado A1 receptor antagonist, but was unaffected by 3,7-dimeth

158 protein kinase A inhibitor and an adenosine A1 receptor antagonist.

159 nized by 8-phenyltheophylline (1 microM), an A1 receptor antagonist.

160 ed with either a glial toxin or an adenosine A1 receptor antagonist.

161 lfophenyl theophylline or with the selective A1-receptor antagonist 1,3-dipropyl, 8-cyclopentylxanthi

162 F and volume overload, KW-3902, an adenosine A1-receptor antagonist, enhances the response to loop di

163 is that the use of rolofylline, an adenosine A1-receptor antagonist, would improve dyspnea, reduce th

164 ion were abolished or prevented by adenosine A1 receptor antagonists (50 mumol/L theophylline/1 mumol

165 ling, readily repeatable, and was blocked by A1 receptor antagonists and by adenosine deaminase, sugg

166 Pertinent to this, brief applications of A1 receptor antagonists immediately after theta stimulat

167 pargylxanthine (DMPX), but unaffected by the A1-receptor antagonists 8-cyclopentyl-1,3-dipropylxanthi

168 eizures, a known potential adverse effect of A1-receptor antagonists.

169 After microdialysis perfusion of A1 receptor antisense in the basal forebrain, spontaneou

170 The increased activity at A1 receptors appeared to be attributable to the direct r

171 lic imidazoline antagonists of the adenosine A1 receptor are described.

172 se effects are mediated by A1 receptors, but A1 receptors are expressed in most brain regions, and di

173 These results indicate that adenosine A1 receptors are selectively upregulated during ethanol

174 Adenosine A1 receptor blockade abolished the protection provided b

175 ibition of nucleotide breakdown or adenosine A1 receptor blockade and reduced by apyrase inactivation

176 Thus, A1 receptor blockade enhances and A2a receptor blockade

177 d during P2X receptor blockade with NF279 or A1 receptor blockade with 1,3-dipropyl-8-cyclopentylxant

178 Adenosine A1 receptor blockade with 4.5 mg/kg DPCPX administered i

179 MPX on the induction of LTP during continued A1 receptor blockade with CPT.

180 uate the dose-dependent effects of adenosine A1-receptor blockade on diuresis and renal function in p

181 ability that were almost coincident with the A1 receptor blocked condition; however, mature synapses

182 The A1 receptor blocker DPCPX did not alter autoregulatory b

183 -1, 3-dipropylxanthine (DPCPX) (an adenosine A1 receptor blocker).

184 ed by microperfusing nephrons with adenosine A1 receptor blocker, A1-agonist, or 5'-nucleotidase inhi

185 RPV4 channel, GABAB, as well as an adenosine A1 receptor blocker.

186 us adenosine inhibited glutamate release via A1 receptors but only inhibited ATP release via A2-like

187 Many of these effects are mediated by A1 receptors, but A1 receptors are expressed in most bra

188 thway can be inhibited through activation of A1 receptors by adenosine.

189 ncreased activation of presynaptic adenosine A1 receptors by endogenous adenosine.

190 A1 receptors caused inhibition of both ATP and glutamate

191 Activation of A1 receptors causes inhibition of adenylate cyclase, dec

192 maphorins signal through neuropilin-2/plexin-A1 receptor complexes on post-crossing commissural axons

193 ypothesis that changes in both adenosine and A1 receptor concentrations can capture changes in cognit

194 ctivity, we examined their action on several A1 receptor constructs, including (1) species variants,

195 Adenosine A1 receptor control of the homeostatic regulation of sle

196 the present work, we tested whether blocking A1 receptors could enhance the damage to DAergic and GAB

197 d subsequent heterologous desensitization of A1 receptors could occur, which might limit the cerebrop

198 The K+ efflux resulting from A1-receptor-coupled KATP-channel activation facilitates

199 Since the A1 receptors decrease intracellular-free calcium, this w

200 sults were not associated with variations in A1 receptor densities and may instead reflect regional a

201 middle-aged slices and thereby activates the A1 receptor-dependent LTP reversal effect.

202 oligodeoxynucleotide targeting the adenosine A1 receptor desensitized the animals to subsequent chall

203 Furthermore, M2 and A1 receptors differentially use Galphai2 and Galphao and

204 tions suggest that the upregulation of brain A1 receptors during ethanol withdrawal may represent a c

205 long-term exposure to caffeine did not alter A1 receptor expression at the acupuncture point.

206 e SAN structure, SAN function, and adenosine A1 receptor expression in control (n=17) and 4-month tac

207 affeine during adulthood increased adenosine A1 receptor expression in the NAc, but no other protein

208 anti-nociceptive actions required adenosine A1 receptor expression.

209 ucted to examine the importance of adenosine A1 receptors for the acquisition and expression of hippo

210 this response to adenosine, but deletion of A1 receptors from CA1 neurons had no effect, demonstrati

211 Deletion of A1 receptors from CA3 neurons abolished this response to

212 ht be attributable to the enhanced adenosine A1 receptor function on synaptic transmission, and the d

213 ateral RA regions with the highest adenosine A1 receptor/GIRK4 expression.

214 To inhibit K(ATP) channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hy

215 thiopyrimidines as selective human adenosine A1 receptor (hA1AR) agonists with tunable binding kineti

216 However, blockade of A1 receptors had no effect on BOLD responses and did not

217 Antisense to the A1 receptor suppressed A1 receptor immunoreactivity but did not show any neurot

218 Conversely, over-expression of the cloned A1 receptor in CASMC increases adenosine- and CCPA-induc

219 nse oligonucleotides against the mRNA of the A1 receptor in the magnocellular cholinergic region of t

220 d we sought to explore the role of adenosine A1 receptors in a model of trigeminovascular nociceptive

221 Stimulation of renal adenosine A1 receptors in animal models has resulted in a signific

222 on of emotional (fear) memories by acting on A1 receptors in brain regions underlying fear conditioni

223 The density of A1 receptors in cerebral cortex was significantly increa

224 in barrier, we examine the role of adenosine A1 receptors in mediating cortical blood flow and metabo

225 Our results demonstrate a novel action of A1 receptors in modulating spinal motor activity.

226 vitro studies supported roles for adenosine A1 receptors in promoting fatty acid synthesis and for A

227 he concentrations of adenosine and adenosine A1 receptors in specific regions of the brain.

228 ector to focally delete endogenous adenosine A1 receptors in the hippocampus.

229 evel but not of K(ATP) channels or adenosine A1 receptors in the preconditioning effects of CSD.

230 ence supporting the involvement of adenosine A1 receptors in the regulation of the response of the ci

231 HVR), and investigated the role of adenosine A1 receptors in these SF effects in conscious adult male

232 ur hypothesis that adenosine, acting via the A1 receptor, in the basal forebrain is a key component i

233 This effect requires functional adenosine A1 receptors, in line with the observation that ATP is r

234 eceptor blockade in the presence of complete A1 receptor inhibition led to a reversible reduction of

235 .5 mM), but was not affected by an adenosine A1 receptor inhibitor, 8-cyclopentyl-1,3-dipropylxanthin

236 receptors and to decrease metabolic rate via A1 receptors inside the blood brain barrier.

237 me in the mammalian fetus that the adenosine A1 receptor is an important mediator of brain metabolic

238 oxygen consumption, suggesting the adenosine A1 receptor is involved in lowering metabolic rate durin

239 ing its cardioprotective effect, whereas the A1 receptor is linked via Gi to phospholipase C to produ

240 d indicate that LPA signaling through the LP(A1) receptor is required for normal development of an in

241 hypothesized that adenosine, acting via the A1 receptor, is a key factor in the homeostatic control

242 e is largely mediated by adenosine acting on A1 receptors, lead us to propose that adenosine is relea

243 3-kinase/AKT pathways primarily through the A1 receptor, leading to CASMC mitogenesis.

244 ccompanies sleep deprivation, acting via the A1 receptor, led to activation of the transcription fact

245 e include A2-receptor mediated vasodilation, A1-receptor mediated improvement of glycolysis during is

246 er, the cell-signaling mechanisms underlying A1 receptor-mediated CASMC proliferation in response to

247 rs with Cl-IB-MECA antagonized the adenosine A1 receptor-mediated inhibition of excitatory neurotrans

248 data provide good evidence for an adenosine A1 receptor-mediated inhibition of mAChR-mediated synapt

249 does not appear to be involved in adenosine A1 receptor-mediated inhibition of neuronal firing.

250 n addition, hydroxylamine reversed adenosine A1 receptor-mediated inhibition of the evoked population

251 ing extracellular adenosine, a loss of tonic A1 receptor-mediated inhibition.

252 n of a two-pore domain potassium channel and A1 receptor-mediated opening of a G-protein-coupled inwa

253 on and cardioprotection but had no effect on A1 receptor-mediated phospholipase C activation or cardi

254 h MRS 1191, which by itself had no effect on A1 receptor-mediated responses.

255 n increased both adenosine concentration and A1 receptor-mediated synaptic inhibition.

256 Agents that inhibit adenosine A1 receptors might be useful in the treatment of MTX-ind

257 Adenosine A1 receptors modulate baseline synaptic transmission in

258 e A1 receptor, this AAV-Cre markedly reduced A1 receptor mRNA and focally abolished the postsynaptic

259 s directly reduces tremor, whereas adenosine A1 receptor-null mice show involuntary movements and sei

260 the sign of Sema6D and signals Nr-CAM/Plexin-A1 receptors on RGCs to implement the contralateral RGC

261 However, during chemical ischemia, the A1 receptor pathway rapidly became ineffective.

262 tor was cloned and expressed in COS-1 cells, A1 receptor pharmacology is confirmed.

263 endogenous adenosine acting at the neuronal A1 receptor plays a major role in the depression of syna

264 ow that blocking the activation of adenosine A1 receptors prevents the long-term depression (LTD) evo

265 s study revealed a 3-fold RA-to-LA adenosine A1 receptor protein expression gradient in the human hea

266 Adenosine A1 receptor protein expression was significantly upregul

267 hese results show that presynaptic GABAB and A1 receptors reduce glutamate and GABA release from nerv

268 fect, but those for adrenergic and adenosine A1 receptors reduced firing.

269 that tonically released adenosine acting on A1 receptors reduces HR in 1CH rats and stimulates endot

270 We used CPA and DPCPX to test whether A1 receptors regulated spinal motor pattern generation i

271 In the presence of DPCPX (50 nM, to block A1 receptors), residual [125I]AB-MECA binding to A2A rec

272 Upon solubilization, the retinal adenosine A1 receptor retained binding characteristics similar to

273 e, because of its ability to block adenosine A1 receptors, shares neurochemical properties with other

274 dnSNARE mice) or pharmacological blockade of A1 receptor signaling using an adenosine A1 receptor (A1

275 ved intravitreal injections of the adenosine A1 receptor stimulant adenosine amine congener (ADAC) or

276 dose-dependent manner and predominantly via A1 receptors, stimulated IP3 receptor-regulated calcium

277 o indicate that muscle dilatation induced by A1 receptor stimulation is entirely NO dependent while t

278 KATP channel opening, while that induced by A1 receptor stimulation is wholly dependent on KATP chan

279 The selectivity level over the adenosine A1 receptor subtype for some of the more active analogue

280 aptic mechanisms involving the activation of A1 receptors suppress tremor activity and limit stimulat

281 Antisense to the A1 receptor suppressed A1 receptor immunoreactivity but

282 ated by a pathway initiated at the adenosine A1 receptor that transduced signals through a Ca2+-activ

283 e results in elevated cell surface levels of A1 receptors, these cells will be more susceptible to ex

284 king the major coding exon for the adenosine A1 receptor, this AAV-Cre markedly reduced A1 receptor m

285 ting that adenosine signals strongly via the A1 receptor to these mitogenic signaling pathways.

286 ously released adenosine acts on endothelial A1 receptors to evoke dilatation in a NO-dependent fashi

287 ing systemic hypoxia and acts on endothelial A1 receptors to open KATP channels on the endothelial ce

288 mediated by adenosine acting at endothelial A1 receptors to stimulate synthesis and release of NO, w

289 In chronic HF, adenosine A1 receptor upregulation in SAN pacemaker and atrial car

290 ain is unlikely to affect the sensitivity of A1 receptors via this mechanism.

291 When a cDNA encoding the porcine A1 receptor was cloned and expressed in COS-1 cells, A1

292 f a postsynaptic K+ conductance by adenosine A1 receptors was used to determine the rate of adenosine

293 In addition, we found that adenosine A1 receptors were required for astrocyte calcium activat

294 As an example we show that the adenosine A1 receptor, when placed under the influence of the mous

295 sine may activate afferent discharge through A1 receptors, while sensitization to BK could involve a

296 Immature and mature synapses expressed A1 receptors with no observable difference in functional

297 potentiate agonist [(3)H]CCPA binding to the A1 receptor, with 4e as the best compound of the series.

298 ,273, which increases adenosine's binding to A1 receptors, would reduce hypoxia-induced brain injury.

299 This A1-receptor-Y(288)A was retained in the ER of stably tra

300 mbination and enhanced surface expression of A1-receptor-Y(288)A within 1 hour.