scholarly journals Role of Adenosine A1 Receptors in Remote Ischemic Preconditioning Protection

2018 ◽  
Vol 86 (2) ◽  
pp. 86-89
Author(s):  
Diamela Paez ◽  
Elina P Bin ◽  
Verónica Casanova ◽  
Eliana Cicale ◽  
Ricardo Gelpi ◽  
...  
Keyword(s):  
Ischemic Preconditioning ◽  
Remote Ischemic Preconditioning ◽  
Adenosine A1 Receptors ◽  
Adenosine A1

The role of adenosine A1 receptors in the interaction between amygdala and entorhinal cortex of kindled rats

2005 ◽  
Vol 65 (1-2) ◽  
pp. 1-9 ◽  
Author(s):  
Mohammad Mohammad-Zadeh ◽  
Azam Amini ◽  
Javad Mirnajafi-Zadeh ◽  
Yaghoub Fathollahi
Keyword(s):  
Entorhinal Cortex ◽  
Adenosine A1 Receptors ◽  
Adenosine A1

scholarly journals Contribution of extrasynaptic N -methyl- d -aspartate and adenosine A1 receptors in the generation of dendritic glutamate-mediated plateau potentials

2015 ◽  
Vol 370 (1672) ◽  
pp. 20140193 ◽  
Author(s):  
Katerina D. Oikonomou ◽  
Mandakini B. Singh ◽  
Matthew T. Rich ◽  
Shaina M. Short ◽  
Srdjan D. Antic
Keyword(s):  
Pyramidal Neurons ◽  
Calcium Influx ◽  
Glutamate Uptake ◽  
Plateau Potentials ◽  
Adenosine A1 Receptors ◽  
Basal Dendrites ◽  
Adenosine A1 ◽  
Dendritic Spikes ◽  
Neuronal Output

Thin basal dendrites can strongly influence neuronal output via generation of dendritic spikes. It was recently postulated that glial processes actively support dendritic spikes by either ceasing glutamate uptake or by actively releasing glutamate and adenosine triphosphate (ATP). We used calcium imaging to study the role of NR2C/D-containing N -methyl- d -aspartate (NMDA) receptors and adenosine A1 receptors in the generation of dendritic NMDA spikes and plateau potentials in basal dendrites of layer 5 pyramidal neurons in the mouse prefrontal cortex. We found that NR2C/D glutamate receptor subunits contribute to the amplitude of synaptically evoked NMDA spikes. Dendritic calcium signals associated with glutamate-evoked dendritic plateau potentials were significantly shortened upon application of the NR2C/D receptor antagonist PPDA, suggesting that NR2C/D receptors prolong the duration of calcium influx during dendritic spiking. In contrast to NR2C/D receptors, adenosine A1 receptors act to abbreviate dendritic and somatic signals via the activation of dendritic K + current. This current is characterized as a slow-activating outward-rectifying voltage- and adenosine-gated current, insensitive to 4-aminopyridine but sensitive to TEA. Our data support the hypothesis that the release of glutamate and ATP from neurons or glia contribute to initiation, maintenance and termination of local dendritic glutamate-mediated regenerative potentials.

Opioids in Remote Ischemic Preconditioning-Induced Cardioprotection

2016 ◽  
Vol 22 (2) ◽  
pp. 112-121 ◽  
Author(s):  
Puneet Kaur Randhawa ◽  
Amteshwar Singh Jaggi
Keyword(s):  
Ischemic Preconditioning ◽  
Ischemia Reperfusion ◽  
Artery Bypass ◽  
Bypass Graft ◽  
Endogenous Opioids ◽  
Remote Ischemic Preconditioning ◽  
Endogenous Opioid System ◽  
Endogenous Opioid ◽  
Cardioprotective Effects

Remote ischemic preconditioning (RIPC) is an intriguing process whereby transient regional ischemia and reperfusion episodes to remote tissues including skeletal, renal, mesenteric provide protection to the heart against sustained ischemia–reperfusion-induced injury. Clinically, this technique has been used in patients undergoing various surgical interventions including coronary artery bypass graft surgery, abdominal aortic aneurysm repair, percutaneous coronary intervention, and heart valve surgery. The endogenous opioid system is extensively expressed in the brain to modulate pain sensation. Besides the role of opioids in relieving pain, numerous researchers have found their critical involvement in evoking cardioprotective effects. Endogenous opioids including endorphins, enkephalins, and dynorphins are released during RIPC and are critically involved in mediating RIPC-induced cardioprotective effects. It has been suggested that during RIPC, the endogenous opioids may be released into the systemic circulation and may travel via bloodstream that act on the myocardial opioid receptors to induce cardioprotection. The present review describes the potential role of opioids in mediating RIPC-induced cardioprotection.

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