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2. Adenosine Receptors and Neuroinflammation

Author

Ferrante, Antonella, De Simone, Roberta, Ajmone-Cat, Maria Antonietta, Minghetti, Luisa, Popoli, Patrizia, Di Giovanni, Giuseppe, Editor-in-Chief, Borea, Pier Andrea, editor, Varani, Katia, editor, Gessi, Stefania, editor, Merighi, Stefania, editor, and Vincenzi, Fabrizio, editor

Published
2018
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12. List of Contributors

Author

Barrachina, Marta, primary, Bernard, Christophe, additional, Bjorness, Theresa E., additional, Blum, David, additional, Boison, Detlev, additional, Chern, Yijuang, additional, Ciruela, Francisco, additional, Coppi, Elisabetta, additional, Cossu, Giovanni, additional, Cristóvão-Ferreira, Sofia, additional, Dettori, Ilaria, additional, Dias, Raquel B., additional, Domenici, Maria R., additional, Fernández-Dueñas, Víctor, additional, Ferrante, Antonella, additional, Ferré, Sergi, additional, Freissmuth, Michael, additional, Fusco, Irene, additional, Geiger, Jonathan D., additional, Greene, Robert W., additional, Klotz, Karl-Norbert, additional, Lin, Chien-Yu, additional, Lopes, Luísa V., additional, Martire, Alberto, additional, Melani, Alessia, additional, de Mendonca, Alexandre, additional, Morelli, Micaela, additional, Pedata, Felicita, additional, Pinna, Annalisa, additional, Plumb, Traci, additional, Popoli, Patrizia, additional, Pousinha, Paula, additional, Pugliese, Anna M., additional, Ribeiro, Joaquim A., additional, Sebastião, Ana M., additional, Tebano, Maria T., additional, Wardas, Jadwiga, additional, and Zappettini, Stefania, additional

Published
2017
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28. Neuroprotective potential of adenosine A 1 receptor partial agonists in experimental models of cerebral ischemia

Author

Martire, Alberto, primary, Lambertucci, Catia, additional, Pepponi, Rita, additional, Ferrante, Antonella, additional, Benati, Nicholas, additional, Buccioni, Michela, additional, Dal Ben, Diego, additional, Marucci, Gabriella, additional, Klotz, Karl‐Norbert, additional, Volpini, Rosaria, additional, and Popoli, Patrizia, additional

Published
2019
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31. Neuroprotective potential of adenosine A1 receptor partial agonists in experimental models of cerebral ischemia.

Author

Martire, Alberto, Lambertucci, Catia, Pepponi, Rita, Ferrante, Antonella, Benati, Nicholas, Buccioni, Michela, Dal Ben, Diego, Marucci, Gabriella, Klotz, Karl‐Norbert, Volpini, Rosaria, and Popoli, Patrizia

Subjects
NEUROPROTECTIVE agents, ADENOSINES, INSULIN agonists, CEREBRAL ischemia, NEUROBLASTOMA
Abstract

Cerebral ischemia is the second most common cause of death and a major cause of disability worldwide. Available therapies are based only on anticoagulants or recombinant tissue plasminogen activator. Extracellular adenosine increases during ischemia and acts as a neuroprotective endogenous agent mainly by activating adenosine A1 receptors (A1Rs) which control calcium influx, glutamate release, membrane potential, and metabolism. Accordingly, in many experimental paradigms it has been already demonstrated that the stimulation of A1R with full agonists is able to reduce ischemia‐related structural and functional brain damage; unfortunately, cardiovascular side effects and desensitization of A1R induced by these compounds have strongly limited their exploitation in stroke therapy so far. Among the newly emerging compounds, A1R partial agonists could be almost free of side effects and equally effective. Therefore, we decided to evaluate the neuroprotective potential of two A1R partial agonists, namely 2′‐dCCPA and 3′‐dCCPA, in in vitro and ex vivo experimental models of cerebral ischemia. Within the experimental paradigm of oxygen‐glucose deprivation in vitro in human neuroblastoma (SH‐SY5Y) cells both A1R partial agonists increased cell viability. Considering the high level of expression of A1Rs in the hippocampus and the susceptibility of CA1 region to hypoxia, we performed electrophysiological experiments in this subfield. The application of 7 min of oxygen‐glucose deprivation constantly produces an irreversible synaptic failure in all the C57Bl/6 mice hippocampal slices evaluated; both tested compounds allowed a significant recovery of synaptic transmission. These findings demonstrate that A1R and its partial agonists are still of interest for cerebral ischemia therapy. [ABSTRACT FROM AUTHOR]

Published
2019
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32. Neuronal adenosine A2A receptor overexpression is neuroprotective towards 3-nitropropionic acid-induced striatal toxicity: a rat model of Huntington’s disease.

Author

Domenici, Maria Rosaria, Chiodi, Valentina, Averna, Mirko, Armida, Monica, Pèzzola, Antonella, Pepponi, Rita, Ferrante, Antonella, Bader, Michael, Fuxe, Kjell, and Popoli, Patrizia

Abstract

The A2A adenosine receptor (A2AR) is widely distributed on different cellular types in the brain, where it exerts a broad spectrum of pathophysiological functions, and for which a role in different neurodegenerative diseases has been hypothesized or demonstrated. To investigate the role of neuronal A2ARs in neurodegeneration, we evaluated in vitro and in vivo the effect of the neurotoxin 3-nitropropionic acid (3-NP) in a transgenic rat strain overexpressing A2ARs under the control of the neural-specific enolase promoter (NSEA2A rats). We recorded extracellular field potentials (FP) in corticostriatal slice and found that the synaptotoxic effect of 3-NP was significantly reduced in NSEA2A rats compared with wild-type animals (WT). In addition, after exposing corticostriatal slices to 3-NP 10 mM for 2 h, we found that striatal cell viability was significantly higher in NSEA2A rats compared to control rats. These in vitro results were confirmed by in vivo experiments: daily treatment of female rats with 3-NP 10 mg/kg for 8 days induced a selective bilateral lesion in the striatum, which was significantly reduced in NSEA2A compared to WT rats. These results demonstrate that the overexpression of the A2AR selectively at the neuronal level reduced 3-NP-induced neurodegeneration, and suggest an important function of the neuronal A2AR in the modulation of neurodegeneration. [ABSTRACT FROM AUTHOR]

Published
2018
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34. Adenosine A2A receptors enable the synaptic effects of cannabinoid CB1 receptors in the rodent striatum.

Author

Tebano, M.-T., Martire, Alberto, Chiodi, Valentina, Pepponi, Rita, Ferrante, Antonella, Domenici, M.-R., Frank, C., Chen, Jiang-Fan, Ledent, Catherine, Popoli, Patrizia, Tebano, M.-T., Martire, Alberto, Chiodi, Valentina, Pepponi, Rita, Ferrante, Antonella, Domenici, M.-R., Frank, C., Chen, Jiang-Fan, Ledent, Catherine, and Popoli, Patrizia

Abstract

Adenosine A(2A), cannabinoid CB(1) and metabotropic glutamate 5 (mGlu(5)) receptors are all highly expressed in the striatum. The aim of the present work was to investigate whether, and by which mechanisms, the above receptors interact in the regulation of striatal synaptic transmission. By extracellular field potentials (FPs) recordings in corticostriatal slices, we demonstrated that the ability of the selective type 1 cannabinoid receptor (CB(1)R) agonist WIN55,212-2 to depress synaptic transmission was prevented by the pharmacological blockade or the genetic inactivation of A(2A)Rs. Such a permissive effect of A(2A)Rs towards CB(1)Rs does not seem to occur pre-synaptically as the ability of WIN55,212-2 to increase the R2/R1 ratio under a protocol of paired-pulse stimulation was not modified by ZM241385. Furthermore, the effects of WIN55,212-2 were reduced in slices from mice lacking post-synaptic striatal A(2A)Rs. The selective mGlu(5)R agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG) potentiated the synaptic effects of WIN55,212-2, and such a potentiation was abolished by A(2A)R blockade. Unlike the synaptic effects, the ability of WIN55,212-2 to prevent NMDA-induced toxicity was not influenced by ZM241385. Altogether, these results show that the state of activation of A(2A)Rs regulates the synaptic effects of CB(1)Rs and that A(2A)Rs may control CB(1) effects also indirectly, namely through mGlu(5)Rs., In Vitro, Journal Article, FLWIN, info:eu-repo/semantics/published

Published
2009

38. Striatal adenosine-cannabinoid receptor interactions in rats over-expressing adenosine A2A receptors.

Author

Chiodi, Valentina, Ferrante, Antonella, Ferraro, Luca, Potenza, Rosa Luisa, Armida, Monica, Beggiato, Sarah, Pèzzola, Antonella, Bader, Michael, Fuxe, Kjell, Popoli, Patrizia, and Domenici, Maria Rosaria

Subjects
*CANNABINOID receptors, *ADENINE, *RIBONUCLEOSIDES, *LABORATORY mice, *ENOLASE
Abstract

Adenosine A2A receptors (A2 ARs) and cannabinoid CB1 receptors ( CB1Rs) are highly expressed in the striatum, where they functionally interact and form A2A/ CB1 heteroreceptor complexes. We investigated the effects of CB1R stimulation in a transgenic rat strain over-expressing A2 ARs under the control of the neural-specific enolase promoter ( NSEA2A rats) and in age-matched wild-type ( WT) animals. The effects of the CB1R agonist WIN 55,212-2 ( WIN) were significantly lower in NSEA2A rats than in WT animals, as demonstrated by i) electrophysiological recordings of synaptic transmission in corticostriatal slices; ii) the measurement of glutamate outflow from striatal synaptosomes and iii) in vivo experiments on locomotor activity. Moreover, while the effects of WIN were modulated by both A2 AR agonist ( CGS 21680) and antagonists ( ZM 241385, KW-6002 and SCH-442416) in WT animals, the A2 AR antagonists failed to influence WIN-mediated effects in NSEA2A rats. The present results demonstrate that in rats with genetic neuronal over-expression of A2 ARs, the effects mediated by CB1R activation in the striatum are significantly reduced, suggesting a change in the stoichiometry of A2A and CB1 receptors and providing a strategy to dissect the involvement of A2 AR forming or not forming heteromers in the modulation of striatal functions. These findings add additional evidence for the existence of an interaction between striatal A2 ARs and CB1Rs, playing a fundamental role in the regulation of striatal functions. [ABSTRACT FROM AUTHOR]

Published
2016
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39. Are there regional variations in the diagnosis surveillance, and control of methicillin-resistant Staphylococcus aureus?

Author

Richet, Hervé, Benbachir, Mohamed, Brown, Derek F., Giamarellou, Helen, Gould, Ian Malcolm, Gubina, Marija, Heczko, Piotr, Kalenic, Smilja, Pana, Marina, Pittet, Didier, Redjeb, Saida Ben, Schindler, Jiri, Starling, Carlos, Struelens, Marc, Witte, Wolfgang, Jarvis, William, Lopardo, Horacio, Rotter, Manfred Ludwig, Ostjic, Maja, Saliba, Jorge, Markova, Boyka, Yuen, Kwok-Yung, Dosso, Mireille, Bencic, Ines, Kucisec-Tepes, Nastja, Skrlin, Jasenta, Susic, Edita, Tomic, Maja, Burgetova, Dagmar, Andre-Richet, Barraud, Dominique, Besnard, Bichier, Edouard, Bingen, M., Branger, Catherine, Cirioni, Anne, Clavel, Stephanie, Clévenot, Simone, Collet, Andréa, Coulomb, François, Courvalin, Patrice, David, Armelle, Denis, François, Ploy, Marie Cécile, Esvant, Jean Yves, Ferrante, Antonella, Genuis, Annick, Guir, Jan, Didier, Jezequel, Françoise, Laborie, Jean Louis, Le Gallou, Florence, Lemoign, Rennes, Christine, Richard, Pascale, Ruellan, Yveline, Vaucel, Jacques, Zbierski, Liliane, Christiansen, Barbel, Fitzner, Julia, Hermann, Mathias, Kramer, Michael, Mathys, Werner, Schubert, Sabine, Weber, Stefan, Katrachoura, A., Papafrangas, Evangelos, Sofianou, Danae, Marton, Anna, Keller, Nathan, Rubinstein, Ethan, Cornaglia, Giuseppe, Perevostikos, Jurjis, Selga, Ivonna, Hemmer, Robert, Alaoui, Mustapha, Benouda-Benjilaji, A., Wagenvoort, Johan, Pytlos, Małgorzata, Hryniewicz, Waleria, Andrei, Manuela Anda, Andries, Dana, Blana, Daniela, Debeleac, Lucia, Dorobat, Olga, Medvetchi-Panatescu, Antonia, Nistor, Irina, Papagheorge, Raluca, Silaghi, Elena, Tudorache, Daniela, Dekhitch, Andrei, Stratchounski, Leonid, Boye, S.B. Cheikh, Seme, Katja, Garau, Javier, Navarro, Ferran, Prats, Guillem, Trilla, Antoni, Richet, Hervé, Benbachir, Mohamed, Brown, Derek F., Giamarellou, Helen, Gould, Ian Malcolm, Gubina, Marija, Heczko, Piotr, Kalenic, Smilja, Pana, Marina, Pittet, Didier, Redjeb, Saida Ben, Schindler, Jiri, Starling, Carlos, Struelens, Marc, Witte, Wolfgang, Jarvis, William, Lopardo, Horacio, Rotter, Manfred Ludwig, Ostjic, Maja, Saliba, Jorge, Markova, Boyka, Yuen, Kwok-Yung, Dosso, Mireille, Bencic, Ines, Kucisec-Tepes, Nastja, Skrlin, Jasenta, Susic, Edita, Tomic, Maja, Burgetova, Dagmar, Andre-Richet, Barraud, Dominique, Besnard, Bichier, Edouard, Bingen, M., Branger, Catherine, Cirioni, Anne, Clavel, Stephanie, Clévenot, Simone, Collet, Andréa, Coulomb, François, Courvalin, Patrice, David, Armelle, Denis, François, Ploy, Marie Cécile, Esvant, Jean Yves, Ferrante, Antonella, Genuis, Annick, Guir, Jan, Didier, Jezequel, Françoise, Laborie, Jean Louis, Le Gallou, Florence, Lemoign, Rennes, Christine, Richard, Pascale, Ruellan, Yveline, Vaucel, Jacques, Zbierski, Liliane, Christiansen, Barbel, Fitzner, Julia, Hermann, Mathias, Kramer, Michael, Mathys, Werner, Schubert, Sabine, Weber, Stefan, Katrachoura, A., Papafrangas, Evangelos, Sofianou, Danae, Marton, Anna, Keller, Nathan, Rubinstein, Ethan, Cornaglia, Giuseppe, Perevostikos, Jurjis, Selga, Ivonna, Hemmer, Robert, Alaoui, Mustapha, Benouda-Benjilaji, A., Wagenvoort, Johan, Pytlos, Małgorzata, Hryniewicz, Waleria, Andrei, Manuela Anda, Andries, Dana, Blana, Daniela, Debeleac, Lucia, Dorobat, Olga, Medvetchi-Panatescu, Antonia, Nistor, Irina, Papagheorge, Raluca, Silaghi, Elena, Tudorache, Daniela, Dekhitch, Andrei, Stratchounski, Leonid, Boye, S.B. Cheikh, Seme, Katja, Garau, Javier, Navarro, Ferran, Prats, Guillem, and Trilla, Antoni

Abstract

SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2003

49. Environmental Fine Particulate Matter (PM 2.5) Activates the RAW 264.7 Macrophage Cell Line Even at Very Low Concentrations as Revealed by 1H NMR

Author

Santini, Maria Teresa, primary, Rainaldi, Gabriella, additional, Ferrante, Antonella, additional, Romano, Rocco, additional, Clemente, Stefania, additional, Motta, Andrea, additional, De Berardis, Barbara, additional, Balduzzi, Maria, additional, Paoletti, Luigi, additional, and Indovina, Pietro Luigi, additional

Published
2003
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