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VOL. 74 (3), 387-408, 2008 FINE TUNING NEUROMODULATION BY ADENOSINE...

CONCLUSIONS

1. Synaptic transmission during neuronal insults is under tight
control of endogenous extracellular adenosine.

2. A1-Receptor minimize the activation of toxic pathways e.g.
inhibiting glutamate release, inhibiting NMDA receptor-
mediated currents, and IL-6 facilitates A1-Receptor inhibition,
and A2A-Receptor interplays with receptors for other
neuromodulators via subtle modifications of fine tuning,
«synchronizing» or «desynchronizing» receptor activation.

3. A2A-Receptors enhance the activity of endogenous
neuroprotective mechanisms e.g. the action of neurotrophic
factors, which are devoted to protect neurons from lesions
(e.g. BDNF, GDNF), so, by A2A receptor activation one can
overcome difficulties found with the use of neurotrophins in
neurodegenerative disorders.

ACKNOWLEDGEMENTS

Laboratory research is currently supported by grants from
Fundação para a Ciência e Tecnologia (FCT), Gulbenkian Foundation
and European Union. I would like to acknowledge colleagues and
collaborators with shared publications: Univ Lisboa (Ana M.
Sebastião, Alexandre de Mendonça), Univ Coimbra (Rodrigo Cunha,
João Malva), Univ Porto (Paulo Correia-de-Sá, Graça Lobo), Univ
Edinburgh (Bernard Ginsborg, Jamieson Walker, Dany McQueen),
Karolinska Inst (Bertil Fredholm), Univ Complutense, Madrid (María
Teresa Miras-Portugal, Esmerilda Delicado), Baylor Coll Med,
Houston (Peter Saggau), Univ Leipzig (Peter Illes), NIH (Sergi Ferré),
Univ Groningen (Knut Biber), Univ Heidelberg (Ulrich Schwabe),
Univ Frankfurt (Herbert Zimmerman), Univ Leiden (Ad Ijzerman),
Univ Murcia (Jesús Hernández), Univ Florence (Felicita Pedata), Univ
Seville (José María Delgado), and Post-docs: Luisa Lopes, Claudia
Valente, Diana Cunha-Reis, and PhD students presently in the lab:
Paula Luís; Natália Assaife-Lopes; Sandra Vaz; Maria José Diógenes;
Catarina Gomes; Ana Rita Costenla; Catarina Fernandes; António
Pinto-Duarte; Raquel Dias; Sofia Ferreira.

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