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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 y formed adenosine can chaperone its cognate A1 receptor.
6 ffinity indistinguishable from the wild-type A1 receptor.
7 indings were recapitulated for the wild-type A1 receptor.
8 ive consequences through a pathway involving A1 receptors.
9  tonically inhibited by adenosine acting via A1 receptors.
10 siently be provoked after blocking adenosine A1 receptors.
11 , metabotropic glutamate mGlu5 and adenosine A1 receptors.
12 ells showed enhanced responses to M2 but not A1 receptors.
13  rescued presynaptic inhibition by adenosine A1 receptors.
14 amidal neurons via activation of presynaptic A1 receptors.
15 vealed greater A2B selectivity over A2A than A1 receptors.
16 ogeneous activation of presynaptic adenosine A1 receptors.
17 ulsant acting on excitatory synapses through A1 receptors.
18 denosine A(2a) receptor versus the adenosine A(1) receptor.
19 is 16 500-fold selective with respect to the A(1) receptor.
20 d an affinity of 7 nM on the human adenosine A(1) receptor.
21 opentyl-1,3-dipropylxanthine (100 nM) at the A(1) receptor.
22 g that the response was mediated entirely by A(1) receptors.
23 ity by adenosine is mediated via presynaptic A(1) receptors.
24 m channels, but involves adenosine acting at A(1) receptors.
25 duced by adenosine in hypoxia is mediated by A(1) receptors.
26 e is mediated by the activation of adenosine A(1) receptors.
27 -X-BY630 dissociation were much lower at the A(1) receptor (1.5-, 1.4-, and 1.5-fold).
28 ateral RA had significantly higher adenosine A1 receptor (2.7+/-1.7-fold; P<0.01) and GIRK4 (1.7+/-0.
29 , Ki=7 nM) and selectivity for the adenosine A1 receptor (915-fold versus adenosine A2A receptor; 12-
30                                    Adenosine A(1) receptor (A(1)AR) agonists have antinociceptive eff
31 hrough sustained activation of the adenosine A(1) receptor (A(1)R) and phospholipase C-mediated deple
32                      Activation of adenosine A(1) receptor (A(1)R) by N(6)-cyclopentidyladenosine (CP
33 ulators of agonist function at the adenosine A(1) receptor (A(1)R) in two different functional assays
34 onate, ACP) directly activated the adenosine A(1) receptor (A(1)R).
35 e(-/-) mice and were eliminated in Adenosine A(1) receptor (A(1)R, Adora1) knock-out mice.
36 y and heart failure, but the contribution of A(1) receptors (A(1)R) and A(3) receptors (A(3)R) is not
37 d by activation of either H(3)R or adenosine A(1) receptors (A(1)R).
38 esis that a partial agonist of the adenosine A1 receptor (A1AdoR) may cause a greater attenuation of
39 is study, we targeted the cochlear adenosine A1 receptor (A1AR) by trans-tympanic injections of the a
40    In this study, we show that the adenosine A1 receptor (A1AR) protects against cisplatin ototoxicit
41                                    Adenosine A1 receptor (A1AR) subtype present on renal proximal tub
42           Allosteric modulation of adenosine A1 receptors (A1ARs) offers a novel therapeutic approach
43                Neurabin attenuated adenosine A(1) receptor (A1R) signaling by assembling a complex be
44  of A1 receptor signaling using an adenosine A1 receptor (A1R) antagonist, 8-cyclopentyl-1,3-dimethyl
45  cortical actin polymerization via adenosine A1 receptor (A1R) induction of a Rho GTPase CDC42-depend
46                                The adenosine A1 receptor (A1R) is a key mediator of the neuroprotecti
47 activity through activation of the adenosine A1 receptor (A1R), resulting in antinociception and high
48  synapses resulting in an enhanced adenosine A1 receptor (A1R)-dependent protective tone despite lowe
49 ate adenosine concentration and/or adenosine A1 receptors (A1R) in the brain.
50           This action is shared by adenosine A(1) receptors (A1Rs), which are also located on Sc term
51 s a neuromodulator acting through inhibitory A1 receptors (A1Rs) and facilitatory A2ARs, which have s
52  The suppression was mediated by presynaptic A1 receptors (A1Rs) because it was blocked by a selectiv
53          Activation of presynaptic adenosine A1 receptors (A1Rs) causes substantial synaptic depressi
54                                    Adenosine A1 receptors (A1Rs) in human and rodent brains can be vi
55 hippocampal neurons, activation of adenosine A1 receptors (A1Rs) or GABA(B) receptors on synaptic ter
56 n mice by increasing activation of adenosine A1 receptors (A1Rs).
57 rosynaptic plasticity; blockade of adenosine A1 receptors abolished it.
58 rosynaptic plasticity: blockade of adenosine A1 receptors abolished weight dependence, while increase
59 n of internal Ca(2+) stores, suggesting that A(1) receptor activation leads to an increase in IP(3),
60  the latter being mediated, in part, through A(1) receptor activation on airway smooth muscle.
61 crotic death, and this can be ameliorated by A(1) receptor activation or A(2A) receptor blockade.
62 n synaptic activity was reduced by adenosine A(1) receptor activation, and a combination of Ca(2+) an
63                                    Adenosine A1 receptor activation also impaired the expression of b
64 fect of acupuncture is mediated by adenosine A1 receptor activation at the acupuncture point, we here
65                                    Adenosine A1 receptor activation depresses excitatory transmission
66                                    Adenosine A1 receptor activation dose-dependently and selectively
67                          However, endogenous A1 receptor activation during cortical seizures in vivo
68      Given the central role demonstrated for A1 receptor activation in determining synaptic amplitude
69 d excitatory neurotransmission via adenosine A1 receptor activation in spinal cord slices from wild-t
70  of trigeminovascular nociception, adenosine A1 receptor activation leads to neuronal inhibition with
71 nal efficacy and therefore the heterogeneous A1 receptor activation seen in the mature neocortex appe
72   Adenosine elicits cardioprotection through A1-receptor activation.
73 we report a novel dual role of the adenosine A1 receptor (Adora1) as an E2/ERalpha target and a regul
74  potential glucagon inhibitor, the adenosine A1 receptor (Adora1), is gradually diminished in alpha-c
75 e thought to require activation of adenosine A1 receptors (adorA1Rs) and release of transmitter molec
76                        After diclofenac, the A(1) receptor agonist CCPA evoked no vasodilatation: we
77 d adult rat ventricular myocytes (ARVM), the A(1) receptor agonist cyclopentyladenosine (CPA) inhibit
78                            Treatment with an A(1) receptor agonist decreases EPSC amplitude and reduc
79                                The adenosine A(1) receptor agonist N(6)-cyclohexyladenosine (CHA) ind
80 hwork cells to the addition of the adenosine A(1) receptor agonist N(6)-cyclohexyladenosine (CHA).
81 ine, N(6)-cyclopentyladenosine (an adenosine A(1) receptor agonist), and 2-[p-(2-carboxyethyl)]phenyl
82 ylxanthine (CPDX; 5 microM and 50 microM) or A(1) receptor agonist, N(6)-cyclopentyladenosine (CPA; 5
83 tion were reduced in mutants treated with an A(1) receptor agonist, whereas an A(2A) receptor agonist
84                                          The A1 receptor agonist 2-Chloro-N6-cyclopentyladenosine (CC
85                                The selective A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CC
86 te receptor antagonist MK-801; the adenosine A1 receptor agonist 2-chloro-N6-cyclopentyladenosine (CC
87     These data are consistent with adenosine A1 receptor agonist actions on REM sleep mediated throug
88  rats were treated IT with the selective Ado A1 receptor agonist cyclohexyladenosine (CHA) or vehicle
89 cholinergic neurons, the selective adenosine A1 receptor agonist N6-cyclohexyladenosine, administered
90                  Microinjection of adenosine A1 receptor agonist or an inhibitor of adenylyl cyclase
91             Direct injection of an adenosine A1 receptor agonist replicated the analgesic effect of a
92 cked by exogenous adenosine or the selective A1 receptor agonist, 2-chloro-N6-cyclopentyl adenosine.
93 lices containing the PnOc incubated with the A1 receptor agonist, cyclohexaladenosine (10(-8) M).
94         The selective low efficacy adenosine A1 receptor agonist, GR190178 (30-1000 microg/kg i.v.),
95 nistration of the highly selective adenosine A1 receptor agonist, GR79236 (3-100 microg/kg) had a dos
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 5.5% with SfA; P<0.001), CCPA (the adenosine A1-receptor agonist, 200 nmol/L) (24.9+/-4.5% versus 54.
99 ts of capadenoson (CAP), a partial adenosine A1-receptor agonist, on left ventricular (LV) function a
100                                              A(1) receptor agonists, but not other purinoceptor-type
101                    Intrathalamic infusion of A1 receptor agonists directly reduces tremor, whereas ad
102 derable literature to suggest that adenosine A1 receptor agonists may have anti-nociceptive effects,
103 tric oxide synthase inhibitors and adenosine A1 receptor agonists.
104 lts support development of partial adenosine A1-receptor agonists for the treatment of chronic heart
105                       Therapy with adenosine A1-receptor agonists, however, is limited by undesirable
106 distributions that spanned those of both the A1 receptor agonized and antagonized conditions.
107                                  Blockade of A1 receptors ameliorated the depression caused by adenos
108        Allosteric enhancers of the adenosine A1 receptor amplify signaling by orthosteric agonists.
109      To confirm the involvement of adenosine A(1) receptors and matrix metalloproteinases (MMP) in an
110 eceptor, dopamine transporter, and adenosine A1 receptor and decreased adenosine A2A receptor express
111 ion was blocked in the presence of adenosine A1 receptor and GABAB receptor blockade.
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 the similar involvement of NMDARs, adenosine A(1) receptors, and PP1 in depotentiation of LTP caused
116 which was prevented by blockade of adenosine A1 receptors, and decreased expression of genes involved
117 racellular Ado, activation of inhibitory Ado A1 receptors, and decreased seizure generation, the desi
118 at is mediated mainly by adenosine acting on A1 receptors, and that the vasoconstrictor effects of sy
119 itive potassium (K(ATP)) channels, adenosine A1 receptors, and the effects of different levels of hal
120 ilocapnic HVR; (2) these impairments require A1 receptors; and (3) SF of OSA may exacerbate OSA via i
121 tor than in those cells expressing the human A1 receptor (ANOVA and posttest comparison, P<0.01).
122                          Moreover, adenosine A1 receptor antagonism had larger effects on theta respo
123 ac arrhythmias and seizures due to adenosine A1-receptor antagonism.
124 LTF (85 +/- 11%, P < 0.05), but an adenosine A(1) receptor antagonist (DPCPX, 3 microg kg(-1), 10 mic
125 tion of MMP-2 was inhibited by the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dimethylxanth
126 yl-adenosine (CPA, 10 nM) and blocked by the A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanth
127  were not altered by the selective adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanth
128 oxic response, is inhibited by the adenosine A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanth
129 t 8-sulphophenyltheopylline (8-SPT), nor the A(1) receptor antagonist 8-cyclopentyl-1,3-dipropylxanth
130                                The adenosine A(1) receptor antagonist 8-cyclopentyltheophylline (CPT)
131                             Furthermore, the A(1) receptor antagonist 8-cyclopentyltheophylline (CPT)
132                                          The A(1) receptor antagonist 8-cyclopentyltheophylline (CPT;
133              Pretreatment with the adenosine A(1) receptor antagonist CPT (10 microM) or the nonselec
134 o characterization of a dual adenosine A(2A)/A(1) receptor antagonist in several animal models of Par
135                 Compound 1 is a potent A(2A)/A(1) receptor antagonist in vitro (A(2A) K(i) = 4.1 nM;
136 quantified after microinjecting an adenosine A(1) receptor antagonist into the prefrontal cortex.
137 inal fluid (aCSF) and two doses of adenosine A(1) receptor antagonist, 1,3-dipropyl-8-phenylxanthine
138 d in preparations treated with the adenosine A(1) receptor antagonist, 8-cyclopentyl-1,3-dimethylxant
139 ion in mutants much more effectively than an A(1) receptor antagonist.
140                                The adenosine A1 receptor antagonist 1,3-dipopylcyclopentylxanthine pr
141 0.9%) by systemic injection of the adenosine A1 receptor antagonist 8-CPT (2.5 mg kg(-1)) approximate
142                           Both the adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin
143 ibitor l-NAME (Group 1, n = 8) and adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin
144                                The adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthin
145  the administration of a selective adenosine A1 receptor antagonist but not by a selective adenosine
146   Since the sleep-suppressing effects of the A1 receptor antagonist CPT were prevented following inhi
147 or administration of the selective adenosine A1 receptor antagonist dipropylcyclopentylxanthine (DPCP
148 ould be inhibited by the selective adenosine A1 receptor antagonist DPCPX (300 microg/kg; P < 0.05).
149                                The adenosine A1 receptor antagonist DPCPX did not affect the resting
150 acerebroventricular infusion of an adenosine A1 receptor antagonist produced a similar decrease in se
151             Here, we show that the adenosine A1 receptor antagonist rolofylline (KW-3902) is alleviat
152  Randomized Study of the Selective Adenosine A1 Receptor Antagonist Rolofylline for Patients Hospital
153 ble to that of BG9928, a selective adenosine A1 receptor antagonist that is currently in clinical tri
154 ropylxanthine (DPCPX), a selective adenosine A1 receptor antagonist that is permeable to the blood br
155    Imidazoline 14 is a competitive adenosine A1 receptor antagonist with a pA2 value of 8.88 and is h
156 (4H)-one, is a particularly potent adenosine A1 receptor antagonist with good selectivity over the ot
157      In the search for a selective adenosine A1 receptor antagonist with greater aqueous solubility t
158  of SPWs in slices treated with an adenosine A1 receptor antagonist, a finding that links the present
159  protein kinase A inhibitor and an adenosine A1 receptor antagonist.
160 ed with either a glial toxin or an adenosine A1 receptor antagonist.
161 F and volume overload, KW-3902, an adenosine A1-receptor antagonist, enhances the response to loop di
162 is that the use of rolofylline, an adenosine A1-receptor antagonist, would improve dyspnea, reduce th
163 sine receptor agonists but adenosine A(2) or A(1) receptor antagonists 3,7-dimethyl-1-propargyl xanth
164                                    Adenosine A(1) receptor antagonists have been used effectively as
165 haracterization of two, dual adenosine A(2A)/A(1) receptor antagonists in several animal models of Pa
166    Compounds 13 and 14 are potent dual A(2A)/A(1) receptor antagonists that have excellent activity,
167 ion were abolished or prevented by adenosine A1 receptor antagonists (50 mumol/L theophylline/1 mumol
168     Pertinent to this, brief applications of A1 receptor antagonists immediately after theta stimulat
169 eizures, a known potential adverse effect of A1-receptor antagonists.
170             After microdialysis perfusion of A1 receptor antisense in the basal forebrain, spontaneou
171              In airway epithelium, A(2B) and A(1) receptors are implicated in the control of Cl(-) an
172 lic imidazoline antagonists of the adenosine A1 receptor are described.
173 se effects are mediated by A1 receptors, but A1 receptors are expressed in most brain regions, and di
174 ncreased neuronal excitability via adenosine A(1) receptors, ATP receptors, and ecto-ATPase.
175              This effect was mediated by the A(1) receptor because pre-treatment with ICB 8-cyclopent
176 eatments, we studied the effect of adenosine A(1) receptor blockade or deletion on bone density.
177 ibition of nucleotide breakdown or adenosine A1 receptor blockade and reduced by apyrase inactivation
178                                        Thus, A1 receptor blockade enhances and A2a receptor blockade
179 d during P2X receptor blockade with NF279 or A1 receptor blockade with 1,3-dipropyl-8-cyclopentylxant
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 RPV4 channel, GABAB, as well as an adenosine A1 receptor blocker.
184 IRK channel activation mediated by adenosine A(1) receptors, but not GABA(B) receptors.
185        Many of these effects are mediated by A1 receptors, but A1 receptors are expressed in most bra
186 resence of a tonic activation of presynaptic A(1) receptors by endogenous adenosine.
187 thway can be inhibited through activation of A1 receptors by adenosine.
188                                Activation of A1 receptors causes inhibition of adenylate cyclase, dec
189 maphorins signal through neuropilin-2/plexin-A1 receptor complexes on post-crossing commissural axons
190 ypothesis that changes in both adenosine and A1 receptor concentrations can capture changes in cognit
191 ctivity, we examined their action on several A1 receptor constructs, including (1) species variants,
192                                    Adenosine A1 receptor control of the homeostatic regulation of sle
193 the present work, we tested whether blocking A1 receptors could enhance the damage to DAergic and GAB
194                 The K+ efflux resulting from A1-receptor-coupled KATP-channel activation facilitates
195 sults were not associated with variations in A1 receptor densities and may instead reflect regional a
196 middle-aged slices and thereby activates the A1 receptor-dependent LTP reversal effect.
197                          Furthermore, M2 and A1 receptors differentially use Galphai2 and Galphao and
198 long-term exposure to caffeine did not alter A1 receptor expression at the acupuncture point.
199 e SAN structure, SAN function, and adenosine A1 receptor expression in control (n=17) and 4-month tac
200 affeine during adulthood increased adenosine A1 receptor expression in the NAc, but no other protein
201  anti-nociceptive actions required adenosine A1 receptor expression.
202 ucted to examine the importance of adenosine A1 receptors for the acquisition and expression of hippo
203  this response to adenosine, but deletion of A1 receptors from CA1 neurons had no effect, demonstrati
204                                  Deletion of A1 receptors from CA3 neurons abolished this response to
205 ht be attributable to the enhanced adenosine A1 receptor function on synaptic transmission, and the d
206 protein-coupled receptors (GPCRs) (adenosine A(1) receptors, GABA(B) receptors, metabotropic glutamat
207 ateral RA regions with the highest adenosine A1 receptor/GIRK4 expression.
208      To inhibit K(ATP) channels or adenosine A1 receptors, glibenclamide (0.1 mg/kg icv; n = 8), 5-hy
209 tor and good selectivity with respect to the A(1) receptor (&gt;200-fold in some cases).
210 thiopyrimidines as selective human adenosine A1 receptor (hA1AR) agonists with tunable binding kineti
211                         However, blockade of A1 receptors had no effect on BOLD responses and did not
212      Antisense to the A1 receptor suppressed A1 receptor immunoreactivity but did not show any neurot
213 esults suggest that CHU rats have functional A(1) receptors in heart and vasculature, but the release
214  vasodilatation and bradycardia by acting on A(1) receptors in normal (N) rats.
215  bilateral activation as well as blockade of A(1) receptors in the PF-LHA on sleep-wakefulness in fre
216 ce for the existence of functional adenosine A(1) receptors in the trabecular cells and that the acti
217    Conversely, over-expression of the cloned A1 receptor in CASMC increases adenosine- and CCPA-induc
218 nse oligonucleotides against the mRNA of the A1 receptor in the magnocellular cholinergic region of t
219 d we sought to explore the role of adenosine A1 receptors in a model of trigeminovascular nociceptive
220 on of emotional (fear) memories by acting on A1 receptors in brain regions underlying fear conditioni
221 in barrier, we examine the role of adenosine A1 receptors in mediating cortical blood flow and metabo
222  vitro studies supported roles for adenosine A1 receptors in promoting fatty acid synthesis and for A
223 he concentrations of adenosine and adenosine A1 receptors in specific regions of the brain.
224 ector to focally delete endogenous adenosine A1 receptors in the hippocampus.
225 evel but not of K(ATP) channels or adenosine A1 receptors in the preconditioning effects of CSD.
226 ence supporting the involvement of adenosine A1 receptors in the regulation of the response of the ci
227 HVR), and investigated the role of adenosine A1 receptors in these SF effects in conscious adult male
228 ur hypothesis that adenosine, acting via the A1 receptor, in the basal forebrain is a key component i
229    This effect requires functional adenosine A1 receptors, in line with the observation that ATP is r
230  role of adenosine--acting through adenosine A(1) receptors--in renal autoregulation has been clarifi
231 ibition of adenylyl cyclase with GABA(B) and A(1) receptors, indicating that these receptors are loca
232 onists and completely abolished by adenosine A(1) receptor inhibition.
233 .5 mM), but was not affected by an adenosine A1 receptor inhibitor, 8-cyclopentyl-1,3-dipropylxanthin
234 one of the sites where adenosine, acting via A(1) receptors, inhibits PF-LHA neurons to promote sleep
235 receptors and to decrease metabolic rate via A1 receptors inside the blood brain barrier.
236     While activation of inhibitory adenosine A(1) receptors is beneficial in epilepsy, chronic pain a
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           Furthermore, adenosine, acting via A(1) receptors, is important in determining D(O2,crit) a
240  hypothesized that adenosine, acting via the A1 receptor, is a key factor in the homeostatic control
241  protection of PostC was absent in adenosine A(1) receptor knockout mice (34.9+/-2.7%) or bradykinin
242  The bone mineral density (BMD) in adenosine A(1) receptor-knockout (A(1)R-knockout) mice was analyze
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  have shown that the activation of adenosine A(1) receptors lower intraocular pressure primarily by i
246     These results suggest that the adenosine A(1) receptor may be a useful target in treating disease
247  recent evidence suggests that adenosine via A(1) receptors may act on PF-LHA neurons to promote slee
248 that heterologous attenuation of GABA(B) and A(1) receptor-mediated inhibition of adenylyl cyclase wa
249 ne, as measured indirectly as a reduction in A(1) receptor-mediated inhibition of glutamate excitator
250 el role for the PP2A holoenzyme in adenosine A(1) receptor-mediated regulation of NHE1 activity in AR
251 se results are considered in relation to the A(1)-receptor-mediated muscle dilatation evoked by syste
252 er, the cell-signaling mechanisms underlying A1 receptor-mediated CASMC proliferation in response to
253 ing extracellular adenosine, a loss of tonic A1 receptor-mediated inhibition.
254 n of a two-pore domain potassium channel and A1 receptor-mediated opening of a G-protein-coupled inwa
255 n increased both adenosine concentration and A1 receptor-mediated synaptic inhibition.
256                                    Adenosine A1 receptors modulate baseline synaptic transmission in
257 e A1 receptor, this AAV-Cre markedly reduced A1 receptor mRNA and focally abolished the postsynaptic
258 s directly reduces tremor, whereas adenosine A1 receptor-null mice show involuntary movements and sei
259  analysis revealed the presence of adenosine A(1) receptors on trigeminal neurons.
260 the sign of Sema6D and signals Nr-CAM/Plexin-A1 receptors on RGCs to implement the contralateral RGC
261 tor was cloned and expressed in COS-1 cells, A1 receptor pharmacology is confirmed.
262  endogenous adenosine acting at the neuronal A1 receptor plays a major role in the depression of syna
263 ow that blocking the activation of adenosine A1 receptors prevents the long-term depression (LTD) evo
264 s study revealed a 3-fold RA-to-LA adenosine A1 receptor protein expression gradient in the human hea
265                                    Adenosine A1 receptor protein expression was significantly upregul
266 fect, but those for adrenergic and adenosine A1 receptors reduced firing.
267  that tonically released adenosine acting on A1 receptors reduces HR in 1CH rats and stimulates endot
268   Upon solubilization, the retinal adenosine A1 receptor retained binding characteristics similar to
269 ropylxanthine (DPCPX) (100 ng), an adenosine A(1) receptor selective antagonist, completely abolished
270 otor incoordination in mice by the adenosine A(1) receptor-selective agonist N(6)-cyclohexyladenosine
271 e, because of its ability to block adenosine A1 receptors, shares neurochemical properties with other
272 dnSNARE mice) or pharmacological blockade of A1 receptor signaling using an adenosine A1 receptor (A1
273 P and OT release also appeared to be via the A(1) receptor, since it was reversed by CPT.
274           These actions were mimicked by the A(1) receptor-specific agonist, N(6)-cyclopentyl-adenosi
275 herefore conclude that adenosine, acting via A(1) receptors, specifically blocks the terminal N-type
276  dose-dependent manner and predominantly via A1 receptors, stimulated IP3 receptor-regulated calcium
277                                    Adenosine A(1) receptor stimulation inhibits this response through
278 ates neuroprotection by activating adenosine A(1) receptor subtype (A(1)AR) linked to suppression of
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 temic hypoxia, adenosine acts on endothelial A(1) receptors to increase PG synthesis, thereby generat
286 ting that adenosine signals strongly via the A1 receptor to these mitogenic signaling pathways.
287 ously released adenosine acts on endothelial A1 receptors to evoke dilatation in a NO-dependent fashi
288  mediated by adenosine acting at endothelial A1 receptors to stimulate synthesis and release of NO, w
289 ent, we could detect little or no inhibitory A(1) receptor tone in basal conditions and during trains
290                     In chronic HF, adenosine A1 receptor upregulation in SAN pacemaker and atrial car
291  However, G protein activation by GABA(B) or A(1) receptors was unaffected.
292             When a cDNA encoding the porcine A1 receptor was cloned and expressed in COS-1 cells, A1
293 oval was required to prevent ouabain-SD when A(1) receptors were blocked.
294     As an example we show that the adenosine A1 receptor, when placed under the influence of the mous
295 glion cells is produced by the activation of A(1) receptors, which initiates a signaling cascade that
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 esults provide novel evidence that adenosine A(1) receptors within the prefrontal cortex comprise par
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.

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