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1 uld be ameliorated by blocking the adenosine A1 receptor.
2 ed by PD81723, an allosteric enhancer of the A1 receptor.
3 y DPCPX, indicating a prominent role for the A1 receptor.
4 ow are mediated by adenosine but not via the 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 , metabotropic glutamate mGlu5 and adenosine A1 receptors.
11 ells showed enhanced responses to M2 but not A1 receptors.
12 rescued presynaptic inhibition by adenosine A1 receptors.
13 vealed greater A2B selectivity over A2A than A1 receptors.
14 adenosine (CPA) it appears to be mediated by A1 receptors.
15 thanol is mediated through myocyte adenosine A1 receptors.
16 y C fibre terminals through an activation of A1 receptors.
17 appears to be due to activation of adenosine A1 receptors.
18 stimulate PRL release in vitro by activating A1 receptors.
19 hypoxia induces dilatation only by acting on A1 receptors.
20 nglia, probably by activation of presynaptic A1 receptors.
21 tion of cAMP formation through activation of A1 receptors.
22 amidal neurons via activation of presynaptic A1 receptors.
23 nd/or A2B but excluding the participation of A1 receptors.
24 A binding could be attributed to labeling of A1 receptors.
25 tion through activation of central adenosine A1 receptors.
26 ogeneous activation of presynaptic adenosine A1 receptors.
27 ulsant acting on excitatory synapses through A1 receptors.
28 ive consequences through a pathway involving A1 receptors.
29 tonically inhibited by adenosine acting via A1 receptors.
30 siently be provoked after blocking adenosine 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-
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
42 of A1 receptor signaling using an adenosine A1 receptor (A1R) antagonist, 8-cyclopentyl-1,3-dimethyl
43 cortical actin polymerization via adenosine A1 receptor (A1R) induction of a Rho GTPase CDC42-depend
45 activity through activation of the adenosine A1 receptor (A1R), resulting in antinociception and high
46 synapses resulting in an enhanced adenosine A1 receptor (A1R)-dependent protective tone despite lowe
48 s a neuromodulator acting through inhibitory A1 receptors (A1Rs) and facilitatory A2ARs, which have s
49 The suppression was mediated by presynaptic A1 receptors (A1Rs) because it was blocked by a selectiv
52 Because very little is known about adenosine A1 receptors (A1Rs) in the spinal cord, we determined th
53 hippocampal neurons, activation of adenosine A1 receptors (A1Rs) or GABA(B) receptors on synaptic ter
56 rosynaptic plasticity: blockade of adenosine A1 receptors abolished weight dependence, while increase
58 fect of acupuncture is mediated by adenosine A1 receptor activation at the acupuncture point, we here
64 d excitatory neurotransmission via adenosine A1 receptor activation in spinal cord slices from wild-t
65 of trigeminovascular nociception, adenosine A1 receptor activation leads to neuronal inhibition with
66 nal efficacy and therefore the heterogeneous A1 receptor activation seen in the mature neocortex appe
68 mical property of dipole and selects against A1 receptor activity, generated a correlated final model
69 we report a novel dual role of the adenosine A1 receptor (Adora1) as an E2/ERalpha target and a regul
70 potential glucagon inhibitor, the adenosine A1 receptor (Adora1), is gradually diminished in alpha-c
71 e thought to require activation of adenosine A1 receptors (adorA1Rs) and release of transmitter molec
72 te receptor antagonist MK-801; the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CC
76 stantial increase in CoRCF and CoVC, but the A1 receptor agonist 2-chloro-N6-cyclopentyladenosine had
77 ) receptor agonist baclofen or the adenosine A1 receptor agonist 2-chloroadenosine, short-term synapt
78 These data are consistent with adenosine A1 receptor agonist actions on REM sleep mediated throug
79 or sodium nitroprusside (SNP), the adenosine A1 receptor agonist CCPA (2-chloro-N6-cyclopentyladenosi
80 rats were treated IT with the selective Ado A1 receptor agonist cyclohexyladenosine (CHA) or vehicle
81 Intrastriatal microinfusion of adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA) and ant
82 cholinergic neurons, the selective adenosine A1 receptor agonist N6-cyclohexyladenosine, administered
83 was mimicked by perfusion with the adenosine A1 receptor agonist N6-cyclopentyladenosine and prevente
88 cked by exogenous adenosine or the selective A1 receptor agonist, 2-chloro-N6-cyclopentyl adenosine.
89 lices containing the PnOc incubated with the A1 receptor agonist, cyclohexaladenosine (10(-8) M).
91 nistration of the highly selective adenosine A1 receptor agonist, GR79236 (3-100 microg/kg) had a dos
93 ystemic injection of the selective adenosine A1 receptor agonist, N(6)-cyclohexyladenosine (CHA; 0.3
94 In Experiment 1, the selective adenosine A1 receptor agonist, N6-cyclopentyladenosine (CPA), or s
95 ould be demonstrated only with the selective A1-receptor agonist 2-chloro-N6-cyclopentyladenosine and
97 5.5% with SfA; P<0.001), CCPA (the adenosine A1-receptor agonist, 200 nmol/L) (24.9+/-4.5% versus 54.
98 cement of [3H]DPCPX binding by the selective A1-receptor agonist, N6-p-sulfophenyladenosine (SPA), yi
99 ts of capadenoson (CAP), a partial adenosine A1-receptor agonist, on left ventricular (LV) function a
102 derable literature to suggest that adenosine A1 receptor agonists may have anti-nociceptive effects,
104 lts support development of partial adenosine A1-receptor agonists for the treatment of chronic heart
110 eceptor, dopamine transporter, and adenosine A1 receptor and decreased adenosine A2A receptor express
112 were combined with homology modeling of the A1 receptor and in silico screening of an allosteric enh
113 A areas with highest expression of adenosine A1 receptor and its downstream GIRK (G protein-coupled i
114 (R)-phenylisopropyl]adenosine from rat brain A1 receptors and [3H]2-[p-(2-carboxyethyl)phenyl-ethylam
115 ments using [3H]cyclohexyladenosine to label A1 receptors and [3H]CGS 21680 to label A2A receptors.
116 produced up-regulation of central adenosine A1 receptors and created a state of opiate dependence, w
117 M, respectively, at the rat and cloned human A1-receptors and with 1800-fold (rat) and 2400-fold (hum
118 which was prevented by blockade of adenosine A1 receptors, and decreased expression of genes involved
119 racellular Ado, activation of inhibitory Ado A1 receptors, and decreased seizure generation, the desi
120 at is mediated mainly by adenosine acting on A1 receptors, and that the vasoconstrictor effects of sy
121 itive potassium (K(ATP)) channels, adenosine A1 receptors, and the effects of different levels of hal
122 ilocapnic HVR; (2) these impairments require A1 receptors; and (3) SF of OSA may exacerbate OSA via i
123 tor than in those cells expressing the human A1 receptor (ANOVA and posttest comparison, P<0.01).
126 xogenous adenosine, or a selective adenosine A1 receptor antagonist (8-cyclopentyl-1, 3-dimethylxanth
128 0.9%) by systemic injection of the adenosine A1 receptor antagonist 8-CPT (2.5 mg kg(-1)) approximate
129 ly reversed in the presence of the adenosine A1 receptor antagonist 8-cyclopentyl-1, 3-dipropylxanthi
131 ibitor l-NAME (Group 1, n = 8) and adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin
133 s a mediator of IPC, the selective adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin
137 the administration of a selective adenosine A1 receptor antagonist but not by a selective adenosine
138 Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhi
139 or administration of the selective adenosine A1 receptor antagonist dipropylcyclopentylxanthine (DPCP
140 arge induced by adenosine was blocked by the A1 receptor antagonist DPCPX (10 microM) but remained un
141 ould be inhibited by the selective adenosine A1 receptor antagonist DPCPX (300 microg/kg; P < 0.05).
142 fter administration of a selective adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropyl
143 .4 nM for antagonism of CPA by the adenosine A1 receptor antagonist DPCPX (8-cyclopentyl-1,3-dipropyl
146 acerebroventricular infusion of an adenosine A1 receptor antagonist produced a similar decrease in se
148 Randomized Study of the Selective Adenosine A1 Receptor Antagonist Rolofylline for Patients Hospital
149 ble to that of BG9928, a selective adenosine A1 receptor antagonist that is currently in clinical tri
150 ropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist that is permeable to the blood br
151 Imidazoline 14 is a competitive adenosine A1 receptor antagonist with a pA2 value of 8.88 and is h
152 (4H)-one, is a particularly potent adenosine A1 receptor antagonist with good selectivity over the ot
153 In the search for a selective adenosine A1 receptor antagonist with greater aqueous solubility t
154 of SPWs in slices treated with an adenosine A1 receptor antagonist, a finding that links the present
155 y 1,3-dipropyl-8-cyclopentylxanthine, an Ado A1 receptor antagonist, but was unaffected by 3,7-dimeth
159 lfophenyl theophylline or with the selective A1-receptor antagonist 1,3-dipropyl, 8-cyclopentylxanthi
160 F and volume overload, KW-3902, an adenosine A1-receptor antagonist, enhances the response to loop di
161 is that the use of rolofylline, an adenosine A1-receptor antagonist, would improve dyspnea, reduce th
162 ion were abolished or prevented by adenosine A1 receptor antagonists (50 mumol/L theophylline/1 mumol
163 ling, readily repeatable, and was blocked by A1 receptor antagonists and by adenosine deaminase, sugg
164 Pertinent to this, brief applications of A1 receptor antagonists immediately after theta stimulat
165 pargylxanthine (DMPX), but unaffected by the A1-receptor antagonists 8-cyclopentyl-1,3-dipropylxanthi
170 se effects are mediated by A1 receptors, but A1 receptors are expressed in most brain regions, and di
173 ibition of nucleotide breakdown or adenosine A1 receptor blockade and reduced by apyrase inactivation
175 d during P2X receptor blockade with NF279 or A1 receptor blockade with 1,3-dipropyl-8-cyclopentylxant
179 uate the dose-dependent effects of adenosine A1-receptor blockade on diuresis and renal function in p
180 ability that were almost coincident with the A1 receptor blocked condition; however, mature synapses
183 ed by microperfusing nephrons with adenosine A1 receptor blocker, A1-agonist, or 5'-nucleotidase inhi
185 us adenosine inhibited glutamate release via A1 receptors but only inhibited ATP release via A2-like
191 maphorins signal through neuropilin-2/plexin-A1 receptor complexes on post-crossing commissural axons
192 ypothesis that changes in both adenosine and A1 receptor concentrations can capture changes in cognit
193 ctivity, we examined their action on several A1 receptor constructs, including (1) species variants,
195 the present work, we tested whether blocking A1 receptors could enhance the damage to DAergic and GAB
196 d subsequent heterologous desensitization of A1 receptors could occur, which might limit the cerebrop
200 sults were not associated with variations in A1 receptor densities and may instead reflect regional a
202 oligodeoxynucleotide targeting the adenosine A1 receptor desensitized the animals to subsequent chall
204 s tested (cAMP, AMP, ADP, and ATP) activated A1 receptors directly at the concentrations tested (</=2
205 tions suggest that the upregulation of brain A1 receptors during ethanol withdrawal may represent a c
207 e SAN structure, SAN function, and adenosine A1 receptor expression in control (n=17) and 4-month tac
208 affeine during adulthood increased adenosine A1 receptor expression in the NAc, but no other protein
210 ucted to examine the importance of adenosine A1 receptors for the acquisition and expression of hippo
211 this response to adenosine, but deletion of A1 receptors from CA1 neurons had no effect, demonstrati
213 ht be attributable to the enhanced adenosine A1 receptor function on synaptic transmission, and the d
215 To inhibit K(ATP) channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hy
216 thiopyrimidines as selective human adenosine A1 receptor (hA1AR) agonists with tunable binding kineti
218 Antisense to the A1 receptor suppressed A1 receptor immunoreactivity but did not show any neurot
219 Conversely, over-expression of the cloned A1 receptor in CASMC increases adenosine- and CCPA-induc
220 nse oligonucleotides against the mRNA of the A1 receptor in the magnocellular cholinergic region of t
221 d we sought to explore the role of adenosine A1 receptors in a model of trigeminovascular nociceptive
223 on of emotional (fear) memories by acting on A1 receptors in brain regions underlying fear conditioni
225 in barrier, we examine the role of adenosine A1 receptors in mediating cortical blood flow and metabo
227 vitro studies supported roles for adenosine A1 receptors in promoting fatty acid synthesis and for A
230 evel but not of K(ATP) channels or adenosine A1 receptors in the preconditioning effects of CSD.
231 ence supporting the involvement of adenosine A1 receptors in the regulation of the response of the ci
232 HVR), and investigated the role of adenosine A1 receptors in these SF effects in conscious adult male
233 ur hypothesis that adenosine, acting via the A1 receptor, in the basal forebrain is a key component i
234 This effect requires functional adenosine A1 receptors, in line with the observation that ATP is r
235 eceptor blockade in the presence of complete A1 receptor inhibition led to a reversible reduction of
236 .5 mM), but was not affected by an adenosine A1 receptor inhibitor, 8-cyclopentyl-1,3-dipropylxanthin
238 me in the mammalian fetus that the adenosine A1 receptor is an important mediator of brain metabolic
239 oxygen consumption, suggesting the adenosine A1 receptor is involved in lowering metabolic rate durin
240 ing its cardioprotective effect, whereas the A1 receptor is linked via Gi to phospholipase C to produ
241 d indicate that LPA signaling through the LP(A1) receptor is required for normal development of an in
242 hypothesized that adenosine, acting via the A1 receptor, is a key factor in the homeostatic control
243 e is largely mediated by adenosine acting on A1 receptors, lead us to propose that adenosine is relea
245 ccompanies sleep deprivation, acting via the A1 receptor, led to activation of the transcription fact
246 e include A2-receptor mediated vasodilation, A1-receptor mediated improvement of glycolysis during is
247 er, the cell-signaling mechanisms underlying A1 receptor-mediated CASMC proliferation in response to
248 rs with Cl-IB-MECA antagonized the adenosine A1 receptor-mediated inhibition of excitatory neurotrans
249 data provide good evidence for an adenosine A1 receptor-mediated inhibition of mAChR-mediated synapt
251 n addition, hydroxylamine reversed adenosine A1 receptor-mediated inhibition of the evoked population
253 n of a two-pore domain potassium channel and A1 receptor-mediated opening of a G-protein-coupled inwa
254 on and cardioprotection but had no effect on A1 receptor-mediated phospholipase C activation or cardi
259 e A1 receptor, this AAV-Cre markedly reduced A1 receptor mRNA and focally abolished the postsynaptic
260 s directly reduces tremor, whereas adenosine A1 receptor-null mice show involuntary movements and sei
261 the sign of Sema6D and signals Nr-CAM/Plexin-A1 receptors on RGCs to implement the contralateral RGC
264 endogenous adenosine acting at the neuronal A1 receptor plays a major role in the depression of syna
265 ow that blocking the activation of adenosine A1 receptors prevents the long-term depression (LTD) evo
266 s study revealed a 3-fold RA-to-LA adenosine A1 receptor protein expression gradient in the human hea
268 hese results show that presynaptic GABAB and A1 receptors reduce glutamate and GABA release from nerv
270 that tonically released adenosine acting on A1 receptors reduces HR in 1CH rats and stimulates endot
272 In the presence of DPCPX (50 nM, to block A1 receptors), residual [125I]AB-MECA binding to A2A rec
273 Upon solubilization, the retinal adenosine A1 receptor retained binding characteristics similar to
274 e, because of its ability to block adenosine A1 receptors, shares neurochemical properties with other
275 dnSNARE mice) or pharmacological blockade of A1 receptor signaling using an adenosine A1 receptor (A1
276 ved intravitreal injections of the adenosine A1 receptor stimulant adenosine amine congener (ADAC) or
277 dose-dependent manner and predominantly via A1 receptors, stimulated IP3 receptor-regulated calcium
278 o indicate that muscle dilatation induced by A1 receptor stimulation is entirely NO dependent while t
279 KATP channel opening, while that induced by A1 receptor stimulation is wholly dependent on KATP chan
280 The selectivity level over the adenosine A1 receptor subtype for some of the more active analogue
281 aptic mechanisms involving the activation of A1 receptors suppress tremor activity and limit stimulat
283 ated by a pathway initiated at the adenosine A1 receptor that transduced signals through a Ca2+-activ
284 e results in elevated cell surface levels of A1 receptors, these cells will be more susceptible to ex
285 king the major coding exon for the adenosine A1 receptor, this AAV-Cre markedly reduced A1 receptor m
287 ously released adenosine acts on endothelial A1 receptors to evoke dilatation in a NO-dependent fashi
288 ing systemic hypoxia and acts on endothelial A1 receptors to open KATP channels on the endothelial ce
289 mediated by adenosine acting at endothelial A1 receptors to stimulate synthesis and release of NO, w
293 f a postsynaptic K+ conductance by adenosine A1 receptors was used to determine the rate of adenosine
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
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.
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