Adenosine in the neurobiology of schizophrenia: potential adenosine receptor-based pharmacotherapy

Francisco Ciruela*, Víctor Fernández-Dueñas, Fernando Contreras, Josep M. Arnau, José Manuel Menchón, Antoni Vallano

*Corresponding author for this work

Research output: Chapter in BookChapterResearch

2 Citations (Scopus)

Abstract

The pharmacological treatment of schizophrenia is currently based on restoring striatal dopamine and prefrontal cortex glutamate neurotransmission. However, these therapies are usually insufficient to completely manage all disease symptoms (i.e., negative and cognitive symptoms). Thus, the study of alternative and/or complementary neurotransmitter systems, which might impinge onto the etiology of schizophrenia, constitutes a big challenge for modern neuropsychiatry. Adenosine is a well known neuromodulator in the central nervous system (CNS) with beneficial properties for a number of brain disorders. The physiological effects of this nucleoside are mediated by G protein-coupled adenosine receptors, which have clearly evolved as drug targets for the pharmacotherapy of certain CNS diseases (e.g., Parkinson disease). Interestingly, it has been demonstrated that adenosine is able to modulate not only the dopaminergic but also glutamatergic system, thus representing a promising candidate to restore the schizophrenia-associated dopamine-glutamate imbalance that may underlie the origins of the disease. Accordingly, the development of drugs targeting adenosine receptors will constitute a worthwhile challenge for current neuropharmacology, because these compounds will definitively enrich the pharmacological arsenal and the pharmacotherapeutic opportunities surrounding schizophrenia. Keywords Adenosine Adenosine receptors Schizophrenia

Original languageEnglish
Title of host publicationPsychiatry and Neuroscience Update. Bridging the divide. Gargiulo, P.A. & Mesones, H.L. Eds.
Place of PublicationCham (CH)
Pages375-388
Number of pages14
Edition1
ISBN (Electronic)9783319171036
DOIs
Publication statusPublished - 1 Jan 2015

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