Utilize este identificador para referenciar este registo: http://hdl.handle.net/10451/7378
Título: Cross talk between A1 and A2A adenosine receptors in the hippocampus and cortex of young adult and old rats
Autor: Lopes, Luísa V.
Cunha, Rodrigo A.
Ribeiro, J.
Palavras-chave: Adenosine receptors
A1 and A2A adenosine receptors
Data: 1999
Editora: American Physiological Society
Citação: J. Neurophysiol. 82: 3196–3203, 1999
Resumo: Adenosine modulates synaptic transmission by acting on inhibitory A1 and facilitatory A2A receptors, the densities of which are modified in aged animals. We investigated how A2A receptor activation influences A1 receptor function and whether this interaction is modified in aged rats. In hippocampal and cortical nerve terminals from young adult (6 wk), but not old rats (24 mo), the A2A receptor agonist, 2-[4-(2-carboxyethyl) phenethylamino]-59-N-ethylcarboxamidoadenosine (CGS 21680; 30 μM) decreased the binding affinity of a selective A1 receptor agonist, cyclopentyladenosine (CPA), an effect prevented by the A2A antagonist, (4-(2-[7-amino-2-(2-furyl {1,2,4}- triazolo{2,3-a {1,3,5}triazin-5-yl-aminoethyl)phenol (ZM 241385, 20 nM). This effect of CGS 21680 required intact nerve terminals and was also observed in the absence of Ca2+ This A2A-induced “desensitization” of A1 receptors was prevented by the protein kinase C inhibitor, chelerythrine (6 μM), and was not detected in the presence of the protein kinase C activator, phorbol-12,13-didecanoate (250 nM), which itself caused a reduction in binding affinity for CPA. The protein kinase A inhibitor, N-(2-guanidinoethyl)-5-isoquinolinesulfonamide (10 μM), and the protein kinase A activator, 8-Br-cAMP (1 mM), had no effects on the A2A-induced A1 receptor desensitization. This A2A-induced A1 receptor desensitization had a functional correlation because CGS 21680 (10 nM) attenuated by 40% the inhibition caused by CPA (10 nM) on CA1 area population spike amplitude in hippocampal slices. This A2A/A1 interaction may explain the attenuation by adenosine deaminase (2 U/ml), which removes tonic A1 inhibition, of the facilitatory effect of CGS 21680 on synaptic transmission. The requirement of tonic A1 receptor activation for CGS 21680 to induce facilitation of synaptic transmission was reinforced by the observation that the A1 receptor antagonist, 1,3-dipropyl-8- cyclopentylxanthine (20 nM) prevented CGS 21680 (10 nM) facilitation of population spike amplitude. The present results show the ability of A2A receptors to control A1 receptor function in a manner mediated by protein kinase C, but not protein kinase A, in young adult but not in aged rats.
Descrição: © 1999 The American Physiological Society
Peer review: yes
URI: http://hdl.handle.net/10451/7378
ISSN: 0022-3077
Versão do Editor: Acesso ao texto integral deste artigo em: http://jn.physiology.org/
Full text access at: http://jn.physiology.org/
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