scholarly journals G Protein Activation in Rat Ponto-Mesencephalic Nuclei is Enhanced By Combined Treatment with a Mu Opioid and an Adenosine A1 Receptor Agonist

SLEEP ◽  
2001 ◽  
Vol 24 (1) ◽  
pp. 52-62 ◽  
Author(s):  
Diana Tanase ◽  
Wilbur A. Martin ◽  
Helen A. Baghdoyan ◽  
Ralph Lydic
Keyword(s):  
G Protein ◽  
Receptor Agonist ◽  
Combined Treatment ◽  
Adenosine A1 Receptor ◽  
Mu Opioid ◽  
Protein Activation ◽  
G Protein Activation ◽  
Adenosine A1 ◽  
A1 Receptor

Adenosine improves recovery of postischemic myocardial function via an adenosine A1 receptor mechanism

1992 ◽  
Vol 263 (5) ◽  
pp. H1460-H1465 ◽  
Author(s):  
R. D. Lasley ◽  
R. M. Mentzer
Keyword(s):  
Receptor Agonist ◽  
Myocardial Function ◽  
Left Ventricular ◽  
Adenosine A1 Receptor ◽  
Extracellular Adenosine ◽  
Adenosine A2 Receptor ◽  
Rat Hearts ◽  
Adenosine A1 ◽  
A1 Receptor ◽  
A2 Receptors

The effects of adenosine in the nonischemic heart have been shown to be mediated via its binding to extracellular adenosine A1 and A2 receptors located predominantly on myocytes and endothelial cells, respectively. We tested the hypothesis that the beneficial effect of adenosine on postischemic myocardial function is mediated via an adenosine A1 receptor mechanism. Isolated rat hearts perfused at constant pressure (85 cmH2O) were subjected to 30 min of global no-flow ischemia (37 degrees C) and 45 min of reperfusion. Hearts treated with adenosine (100 microM) and the adenosine A1 receptor agonist N6-cyclohexyladenosine (CHA; 0.25 microM) recovered 72 +/- 4 and 70 +/- 4% of preischemic left ventricular developed pressures (LVDP), respectively, after 45 min of reperfusion compared with untreated hearts (54 +/- 3% of preischemic LVDP). Adenosine and CHA hearts exhibited greater myocardial ATP contents than control hearts after 10 min of ischemia, but there were no differences in tissue ATP levels after 30 min of ischemia. In contrast, hearts treated with the adenosine A2 receptor agonist phenylaminoadenosine (0.25 microM) failed to demonstrate improved postischemic function (52 +/- 5%). The addition of the A1-selective antagonist 8-cyclopentyl-1,3-dipropylxanthine blocked the cardioprotective effect of adenosine (57 +/- 4%). These results suggest that adenosine enhances postischemic myocardial function via an A1 receptor mechanism.

Adenosine pre- and postsynaptic modulation of glutamate-dependent calcium activity in hypothalamic neurons

1995 ◽  
Vol 74 (5) ◽  
pp. 2150-2162 ◽  
Author(s):  
K. Obrietan ◽  
A. B. Belousov ◽  
H. C. Heller ◽  
A. N. van den Pol
Keyword(s):  
Electrical Activity ◽  
Glutamate Receptor ◽  
Receptor Agonist ◽  
Adenosine A1 Receptor ◽  
Receptor Antagonists ◽  
Hypothalamic Neurons ◽  
Postsynaptic Potentials ◽  
Adenosine A1 ◽  
Hypothalamic Cells ◽  
A1 Receptor

1. Within the hypothalamus, adenosine has been reported to influence temperature regulation, sleep homeostasis, and endocrine secretions. The effects of adenosine on hypothalamic neurons have not been studied at the cellular level. Adenosine (5 nM-30 microM) showed no influence on intracellular Ca2+ or electrical activity in the presence of glutamate receptor antagonists D-2-amino-5-phosphonovalerate and 6-cyano-7-nitroquinoxaline-2,3-dione; consequently, we examined the role of adenosine in modulating the activity of glutamate in cultured hypothalamic neurons (n > 1,700) with fura-2 Ca2+ digital imaging and whole cell patch-clamp electrophysiology in the absence of glutamate receptor block. 2. When glutamate receptors were not blocked, adenosine (1-30 microM) and the selective adenosine A1 receptor agonist N6-cyclopentyl adenosine (CPA; 5 nM-1 microM) caused a large reduction in intracellular Ca2+ and electrical activity, suggesting that glutamate neurotransmission was critical for an effect of adenosine to be detected. Neuronal Ca2+ levels were reversibly depressed by CPA (50 nM), with a maximum depression of 90%, and these effects were blocked by coadministration of the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX). 3. Ca2+ levels in immature neurons before the time of synaptogenesis were not affected by adenosine. Adenosine A1 receptor activation suppressed glutamate-mediated Ca2+ activity in neurons in vitro 8 to 73 days. 4. Adenosine (1 or 10 microM) caused a hyperpolarization of membrane potential and a reduction of large postsynaptic potentials arising from endogenously released glutamate. The administration of low concentrations of CPA (5 nM) decreased the frequency of glutamate-mediated, neuronally synchronized Ca2+ transients and the frequency of postsynaptic potentials. 5. To compare the relative effects of adenosine on hypothalamic neurons with cells from other brain regions, we assayed the effects of CPA on glutamate-mediated Ca2+ in hippocampal and cortical cultures. CPA (50 nM) reversibly depressed glutamate-mediated Ca2+ rises in hypothalamic neurons by 35%, compared with 54% in hippocampal neurons and 46% in cortical neurons. 6. If it does play a functional role, adenosine should be released by hypothalamic cells. In some neurons the adenosine A1 receptor antagonists cyclopentyltheophylline or DPCPX caused an increase in intracellular Ca2+, suggesting that adenosine was secreted by hypothalamic cells, tonically depressing glutamate-enhanced neuronal Ca2+. 7. To determine whether adenosine could exert a postsynaptic effect, we coapplied it with glutamate agonists in the presence of tetrodotoxin. Within subpopulations of hypothalamic neurons, adenosine and CPA either inhibited (18% of total neurons) or potentiated (6% of total neurons) responses to glutamate, N-methyl-D-aspartate, and kainate by > or = 20%. 8. In contrast to the modest effects found in neurons, responses of hypothalamic astrocytes to the application of glutamate or the metabotropic glutamate receptor agonist (+/-)-trans-1-amino-1,3-cyclopentanedicarboxylic acid were strongly potentiated by adenosine (mean +225%) and CPA. 9. Together, these findings suggest that adenosine exerts a major presynaptic effect and a minor postsynaptic effect in the modulation of glutamate neurotransmission in the hypothalamus, where it can play a significant role in blocking a large part of the glutamate-induced Ca2+ rise. In the absence of glutamate transmission, adenosine has relatively little effect on either neuronal intracellular Ca2+ or electrical activity.

scholarly journals Reduction of postischemic brain damage and memory deficits following treatment with the selective adenosine A1 receptor agonist

1996 ◽  
Vol 302 (1-3) ◽  
pp. 43-48 ◽  
Author(s):  
Dag K.J.E. Von Lubitz ◽  
Mark Beenhakker ◽  
Rick C.-S. Lin ◽  
Margaret F. Carter ◽  
Ian A. Paul ◽  
...  
Keyword(s):  
Brain Damage ◽  
Receptor Agonist ◽  
Memory Deficits ◽  
Adenosine A1 Receptor ◽  
Adenosine A1 ◽  
A1 Receptor
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