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18. Pharmacology of adenosine A2A receptors

Author

Ongini, Ennio and Fredholm, Bertil B.

Subjects
Adenosine -- Research, Pharmaceutical research -- Reports, Cell receptors -- Research, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

Adenosine [A.sub.2A] receptors, which have been cloned from several mammalian species, are activated by physiological concentrations of adenosine to stimulate the formation of cAMP and other mediators. The [A.sub.2A] receptors are found on neutrophil leukocytes, platelets, blood vessels and, very abundantly, on some cells in the CNS. In the caudate nucleus they coexist with dopamine [D.sub.2] receptors, and stimulation of [A.sub.2A] receptors causes a decrease in [D.sub.2] receptor-mediated neurotransmission. Thus, drugs that act on [A.sub.2A] receptors can be used to modify dopaminergic neurotransmission known to be important in neurological and psychiatric disorders. In this review, Ennio Ongini and Bertil Fredholm describe how recently developed potent and selective [A.sub.2A] receptor antagonists can be used to delineate the physiological and pathological processes regulated by [A.sub.2A] receptors. Results from in vitro and in vivo pharmacology studies strengthen the notion that [A.sub.2A] receptors are an interesting target for drug development.

Published
1996

34. Disclosing apoptosis in the CNS

Author

Abbracchio, Maria P., Ongini, Ennio, and Memo, Maurizio

Subjects
Cell death -- Research, Central nervous system -- Research, Nervous system -- Degeneration, Neurologic manifestations of general diseases -- Research, Biological sciences, Chemistry, Pharmaceuticals and cosmetics industries
Abstract

The Italian Society of Immunology hosted on Sept 18, 1998, a conference that was devoted to research on the molecular mechanisms of apoptosis in the central nervous system. Attended by some 200 delegates from the academe and industry, the conference attracted contributions from scientists from a number of European research centers. The first part of the conference was devoted to the basic mechanisms of apoptosis while the second part focused on the modulation of apoptosis by neurotransmitters. The third and final part looked at the link between apoptosis and neuropathologies.

Published
1999

36. The role of the D2 dopamine receptor ([D.sub.2]R) in [A.sub.2A] adenosine receptor ([A.sub.2A]R)-mediated behavioral and cellular responses as revealed by [A.sub.2A] and [D.sub.2] receptor knockout mice

Author

Chen, Jiang-Fan, Moratalla, Rosario, Impagnatiello, Francesco, Grandy, David K., Cuellar, Beatriz, Rubinstein, Marcelo, Beilstein, Mark A., Hackett, Elizabeth, Fink, J. Stephen, Low, Malcolm J., Ongini, Ennio, and Schwarzschild, Michael A.

Subjects
Dopamine receptors -- Genetic aspects, Adenosine -- Genetic aspects, Mice as laboratory animals -- Usage, Gene expression -- Research, Science and technology
Abstract

The [A.sub.2A]R is largely coexpressed with [D.sub.2]Rs and enkephalin mRNA in the striatum where it modulates dopaminergic activity. Activation of the [A.sub.2A]R antagonizes [D.sub.2]R-mediated behavioral and neurochemical effects in the basal ganglia through a mechanism that may involve direct [A.sub.2A]R-[D.sub.2]R interaction. However, whether the [D.sub.2]R is required for the [A.sub.2A]R to exert its neural function is an open question. In this study, we examined the role of [D.sub.2]Rs in [A.sub.2A]R-induced behavioral and cellular responses, by using genetic knockout (KO) models (mice deficient in [A.sub.2A]RS or [D.sub.2]Rs or both). Behavioral analysis shows that the [A.sub.2A]R agonist 2-4-(2-carboxyethyl)phenethylamino-5'-N-ethylcarboxamidoadenosine reduced spontaneous as well as amphetamineinduced locomotion in both [D.sub.2] KO and wild-type mice. Conversely, the nonselective adenosine antagonist caffeine and the [A.sub.2A]R antagonist 8-(3-chlorostyryl)caffeine produced motor stimulation in mice lacking the [D.sub.2]R, although the stimulation was significantly attentuated. At the cellular level, [A.sub.2A]R inactivation counteracted the increase in enkephalin expression in striatopallidal neurons caused by [D.sub.2]R deficiency. Consistent with the [D.sub.2] KO phenotype, [A.sub.2A]R inactivation partially reversed both acute [D.sub.2]R antagonist (haloperidol)-induced catalepsy and chronic haloperidol-induced enkephalin mRNA expression. Together, these results demonstrate that [A.sub.2A]RS elicit behavioral and cellular responses despite either the genetic deficiency or pharmacological blockade of [D.sub.2]Rs. Thus, [A.sub.2A]R-mediated neural functions are partially independent of [D.sub.2]Rs. Moreover, endogenous adenosine acting at striatal [A.sub.2A]RS may be most accurately viewed as a facilitative modulator of striatal neuronal activity rather than simply as an inhibitory modulator of [D.sub.2]R neurotransmission.

Published
2001

43. The role of the D2 dopamine receptor (D2R) in A2A adenosine receptor (A2AR)-mediated behavioral and cellular responses as revealed by A2A and D2 receptor knockout mice

Author

Chen, Jiang Fan, Moratalla, Rosario, Impagnatiello, Francesco, Grandy, David K., Cuellar, Beatriz, Rubinstein, Marcelo, Beilstein, Mark A., Hackett, Elizabeth, Fink, J. Stephen, Low, Malcolm J., Ongini, Ennio, and Schwarzschild, Michael A.

Subjects
adenosina, Medicina Básica, CIENCIAS MÉDICAS Y DE LA SALUD, Inmunología, dopamina, purl.org/becyt/ford/3 [https], purl.org/becyt/ford/3.1 [https]
Abstract

The A2AR is largely coexpressed with D2Rs and enkephalin mRNA in the striatum where it modulates dopaminergic activity. Activation of the A2AR antagonizes D2R-mediated behavioral and neurochemical effects in the basal ganglia through a mechanism that may involve direct A2AR-D2R interaction. However, whether the D2R is required for the A2AR to exert its neural function is an open question. In this study, we examined the role of D2Rs in A2AR-induced behavioral and cellular responses, by using genetic knockout (KO) models (mice deficient in A2ARs or D2Rs or both). Behavioral analysis shows that the A2AR agonist 2-4-(2-carboxyethyl)phenethylamino-5′-N-ethylcarboxamidoadenosine reduced spontaneous as well as amphetamine-induced locomotion in both D2 KO and wild-type mice. Conversely, the nonselective adenosine antagonist caffeine and the A2AR antagonist 8-(3-chlorostyryl)caffeine produced motor stimulation in mice lacking the D2R, although the stimulation was significantly attentuated. At the cellular level, A2AR inactivation counteracted the increase in enkephalin expression in striatopallidal neurons caused by D2R deficiency. Consistent with the D2 KO phenotype, A2AR inactivation partially reversed both acute D2R antagonist (haloperidol)-induced catalepsy and chronic haloperidol-induced enkephalin mRNA expression. Together, these results demonstrate that A2ARs elicit behavioral and cellular responses despite either the genetic deficiency or pharmacological blockade of D2Rs. Thus, A2AR-mediated neural functions are partially independent of D2Rs. Moreover, endogenous adenosine acting at striatal A2ARs may be most accurately viewed as a facilitative modulator of striatal neuronal activity rather than simply as an inhibitory modulator of D2R neurotransmission. Fil: Chen, Jiang Fan. Harvard Medical School; Estados Unidos. Massachusetts General Hospital; Estados Unidos Fil: Moratalla, Rosario. Instituto Cajal; España Fil: Impagnatiello, Francesco. Schering-Plough Research Institute; Italia Fil: Grandy, David K.. University of Oregon; Estados Unidos Fil: Cuellar, Beatriz. Instituto Cajal; España Fil: Rubinstein, Marcelo. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina Fil: Beilstein, Mark A.. Harvard Medical School; Estados Unidos. Massachusetts General Hospital; Estados Unidos Fil: Hackett, Elizabeth. Harvard Medical School; Estados Unidos. Massachusetts General Hospital; Estados Unidos Fil: Fink, J. Stephen. Harvard Medical School; Estados Unidos. Massachusetts General Hospital; Estados Unidos. Boston University; Estados Unidos Fil: Low, Malcolm J.. University of Oregon; Estados Unidos Fil: Ongini, Ennio. Schering-Plough Research Institute; Italia Fil: Schwarzschild, Michael A.. Harvard Medical School; Estados Unidos. Massachusetts General Hospital; Estados Unidos

Published
2001

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