Effects of oxygen and glucose deprivation on synaptic transmission in rat dentate gyrus: Role of A2A adenosine receptors

2013 ◽  
Vol 67 ◽  
pp. 511-520 ◽  
Author(s):  
Giovanna Maraula ◽  
Chiara Traini ◽  
Tommaso Mello ◽  
Elisabetta Coppi ◽  
Andrea Galli ◽  
...  
Keyword(s):  
Synaptic Transmission ◽  
Dentate Gyrus ◽  
Adenosine Receptors ◽  
Glucose Deprivation ◽  
Oxygen And Glucose Deprivation ◽  
A2a Adenosine Receptors

scholarly journals Adenosine A1 receptor-mediated protection of mouse hippocampal synaptic transmission against oxygen and/or glucose deprivation: a comparative study

2019 ◽  
Vol 122 (2) ◽  
pp. 721-728 ◽  
Author(s):  
Masahito Kawamura ◽  
David N. Ruskin ◽  
Susan A. Masino
Keyword(s):  
Synaptic Transmission ◽  
Hippocampal Slices ◽  
Glucose Deprivation ◽  
Acute Response ◽  
Recording Conditions ◽  
Receptor Inactivation ◽  
Acute Hippocampal Slices ◽  
Metabolic Stresses ◽  
The Impact

Adenosine receptors are widely expressed in the brain, and adenosine is a key bioactive substance for neuroprotection. In this article, we clarify systematically the role of adenosine A1 receptors during a range of timescales and conditions when a significant amount of adenosine is released. Using acute hippocampal slices obtained from mice that were wild type or null mutant for the adenosine A1 receptor, we quantified and characterized the impact of varying durations of experimental ischemia, hypoxia, and hypoglycemia on synaptic transmission in the CA1 subregion. In normal tissue, these three stressors rapidly and markedly reduced synaptic transmission, and only treatment of sufficient duration led to incomplete recovery. In contrast, inactivation of adenosine A1 receptors delayed and/or lessened the reduction in synaptic transmission during all three stressors and reduced the magnitude of the recovery significantly. We reproduced the responses to hypoxia and hypoglycemia by applying an adenosine A1 receptor antagonist, validating the clear effects of genetic receptor inactivation on synaptic transmission. We found activation of adenosine A1 receptor inhibited hippocampal synaptic transmission during the acute phase of ischemia, hypoxia, or hypoglycemia and caused the recovery from synaptic impairment after these three stressors using genetic mutant. These studies quantify the neuroprotective role of the adenosine A1 receptor during a variety of metabolic stresses within the same recording system. NEW & NOTEWORTHY Deprivation of oxygen and/or glucose causes a rapid adenosine A1 receptor-mediated decrease in synaptic transmission in mouse hippocampus. We quantified adenosine A1 receptor-mediated inhibition during and synaptic recovery after ischemia, hypoxia, and hypoglycemia of varying durations using a genetic mutant and confirmed these findings using pharmacology. Overall, using the same recording conditions, we found the acute response and the neuroprotective ability of the adenosine A1 receptor depended on the type and duration of deprivation event.

scholarly journals Critical Role of Hypoxia and A2A Adenosine Receptors in Liver Tissue-Protecting Physiological Anti-Inflammatory Pathway

2008 ◽  
Vol 14 (3-4) ◽  
pp. 116-123 ◽  
Author(s):  
Alexander Choukèr ◽  
Manfred Thiel ◽  
Dmitriy Lukashev ◽  
Jerrold M. Ward ◽  
Ines Kaufmann ◽  
...  
Keyword(s):  
Adenosine Receptors ◽  
Liver Tissue ◽  
Critical Role ◽  
Inflammatory Pathway ◽  
A2a Adenosine Receptors ◽  
Anti Inflammatory

scholarly journals Activation of NTS A2a adenosine receptors differentially resets baroreflex control of renal vs. adrenal sympathetic nerve activity

2009 ◽  
Vol 296 (4) ◽  
pp. H1058-H1068 ◽  
Author(s):  
Tomoko K. Ichinose ◽  
Donal S. O'Leary ◽  
Tadeusz J. Scislo
Keyword(s):  
Receptor Antagonist ◽  
Adenosine Receptors ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Response Curves ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
A2a Adenosine Receptors ◽  
Stimulation Of

The role of nucleus of solitary tract (NTS) A2a adenosine receptors in baroreflex mechanisms is controversial. Stimulation of these receptors releases glutamate within the NTS and elicits baroreflex-like decreases in mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA), whereas inhibition of these receptors attenuates HR baroreflex responses. In contrast, stimulation of NTS A2a adenosine receptors increases preganglionic adrenal sympathetic nerve activity (pre-ASNA), and the depressor and sympathoinhibitory responses are not markedly affected by sinoaortic denervation and blockade of NTS glutamatergic transmission. To elucidate the role of NTS A2a adenosine receptors in baroreflex function, we compared full baroreflex stimulus-response curves for HR, RSNA, and pre-ASNA (intravenous nitroprusside/phenylephrine) before and after bilateral NTS microinjections of selective adenosine A2a receptor agonist (CGS-21680; 2.0, 20 pmol/50 nl), selective A2a receptor antagonist (ZM-241385; 40 pmol/100 nl), and nonselective A1 + A2a receptor antagonist (8-SPT; 1 nmol/100 nl) in urethane/α-chloralose anesthetized rats. Activation of A2a receptors decreased the range, upper plateau, and gain of baroreflex-response curves for RSNA, whereas these parameters all increased for pre-ASNA, consistent with direct effects of the agonist on regional sympathetic activity. However, no resetting of baroreflex-response curves along the MAP axis occurred despite the marked decreases in baseline MAP. The antagonists had no marked effects on baseline variables or baroreflex-response functions. We conclude that the activation of NTS A2a adenosine receptors differentially alters baroreflex control of HR, RSNA, and pre-ASNA mostly via non-baroreflex mechanism(s), and these receptors have virtually no tonic action on baroreflex control of these sympathetic outputs.

scholarly journals The Mediating Role of A2A Adenosine Receptors in the Mitochondrial Pathway of Apoptotic Hippocampal Cell Death, Following the Administration of MDMA in Rat

2017 ◽  
Vol 8 (4) ◽  
pp. 317-324 ◽  
Author(s):  
Masoomeh Bakhshayesh ◽  
Fereshteh Golab ◽  
Fatemeh Kermanian ◽  
Mehdi Mehdizadeh ◽  
Amir Reza Katebi ◽  
...  
Keyword(s):  
Cell Death ◽  
Adenosine Receptors ◽  
Mitochondrial Pathway ◽  
Mediating Role ◽  
A2a Adenosine Receptors ◽  
Hippocampal Cell

scholarly journals Adenosine A1but Not A2aReceptor Agonist Reduces Hyperalgesia Caused by a Surgical Incision in Rats

2007 ◽  
Vol 107 (5) ◽  
pp. 797-806 ◽  
Author(s):  
Peter K. Zahn ◽  
Heidrun Straub ◽  
Manuel Wenk ◽  
Esther M. Pogatzki-Zahn
Keyword(s):  
Pertussis Toxin ◽  
Adenosine Receptors ◽  
Antinociceptive Effect ◽  
Intrathecal Administration ◽  
Pain Behavior ◽  
Spontaneous Pain ◽  
Withdrawal Threshold ◽  
A2a Adenosine Receptors ◽  
Before And After

Background Activation of A1 adenosine receptors (A1Rs) causes antinociception after nerve injury and inflammation. However, the role of A2a adenosine receptors (A2aRs) for pain processing is less clear. In the current study, the authors investigated the role of spinal adenosine A1Rs and A2aRs for the maintenance of mechanical hyperalgesia in an animal model for postoperative pain. Methods Rats with intrathecal catheters were anesthetized and underwent plantar incision. Spontaneous pain behavior and withdrawal threshold to punctuate stimulation were measured before and after administration of intrathecal R-phenylisopropyl-adenosine (R-PIA; A1R agonist), 2-w p-2-carbonyl-ethyl-phenylethylaminox-5X-N-ethylcarboxami-doadenosine (CGS21680; A2aR agonist), or vehicle. In separate groups of animals, the effects of pertussis toxin, forskolin, glibenclamide, 4-aminopyridine, tetraethylammonium, apamin, charybdotoxin, or margatoxin on R-PIA-induced antinociception were examined. Results Intrathecal administration of 5 nmol R-PIA but not 10 nmol CGS21680 decreased nonevoked spontaneous pain behavior. Furthermore, intrathecal administration of R-PIA but not of CGS21680 increased withdrawal thresholds after incision. Pretreatment with pertussis toxin and administration of forskolin, glibenclamide, 4-aminopyridine, and tetraethylammonium inhibited R-PIA-induced antinociception. In addition, intrathecal administration of apamin, charybdotoxin, or margatoxin did not modify mechanical hypoalgesia mediated by R-PIA. Conclusions Spinal A1Rs but not A2aRs play an important role in the maintenance of nonevoked and evoked pain behaviors after an incision. Furthermore, A1R-induced spinal antinociception is mediated by interactions with pertussis toxin-sensitive G proteins. In addition, the opening of adenosine triphosphate-sensitive K channels but not of calcium-activated potassium channels and voltage-gated Kv1.3 or Kv1.6 channels contribute to the antinociceptive effect of A1R agonists.

scholarly journals Role of A2A adenosine receptors in regulation of opsonized E. coli-induced macrophage function

2007 ◽  
Vol 3 (4) ◽  
pp. 447-452 ◽  
Author(s):  
Balázs Csóka ◽  
Zoltán H. Németh ◽  
Zsolt Selmeczy ◽  
Balázs Koscsó ◽  
Pál Pacher ◽  
...  
Keyword(s):  
Adenosine Receptors ◽  
Macrophage Function ◽  
E Coli ◽  
A2a Adenosine Receptors
Sign in / Sign up

Export Citation Format

Share Document