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J. Biol. Chem., Vol. 275, Issue 48, 37572-37581, December 1, 2000

This Article Full Text Full Text (PDF) All Versions of this Article: 275/48/37572    most recent M003011200v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Cunha, R. A. Articles by Ribeiro, J. A. Search for Related Content PubMed PubMed Citation Articles by Cunha, R. A. Articles by Ribeiro, J. A. Social Bookmarking                      What's this?

Modification by Arachidonic Acid of Extracellular Adenosine Metabolism and Neuromodulatory Action in the Rat Hippocampus^*

Rodrigo Antunes Cunha^§¶, Teresa Almeida, and Joaquim Alexandre Ribeiro

From the  Laboratory of Neurosciences, Faculty of Medicine, and ^§ Department of Chemistry & Biochemistry, Faculty of Sciences, University of Lisbon, 1649-028 Lisbon, Portugal

Adenosine and arachidonate (AA) fulfil opposite modulatory roles, arachidonate facilitating and adenosine inhibiting cellular responses. To understand if there is an inter-play between these two neuromodulatory systems, we investigated the effect of AA on extracellular adenosine metabolism in hippocampal nerve terminals. AA (30 µM) facilitated by 67% adenosine evoked release and by 45% ATP evoked release. These effects were not significantly modified upon blockade of lipooxygenase or cyclooxygenase and were attenuated (52-61%) by the protein kinase C inhibitor, chelerythrine (6 µM). The ecto-5'-nucleotidase inhibitor, ,-methylene ADP (100 µM), caused a larger inhibition (54%) of adenosine release in the presence of AA (30 µM) compared with control (37% inhibition) indicating that the AA-induced extracellular adenosine accumulation is mostly originated from an increased release and extracellular catabolism of ATP. This AA-induced extracellular adenosine accumulation is further potentiated by an AA-induced decrease (48%) of adenosine transporters capacity. AA (30 µM) increased by 36-42% the tonic inhibition by endogenous extracellular adenosine of adenosine A₁ receptors in the modulation of acetylcholine release and of CA1 hippocampal synaptic transmission in hippocampal slices. These results indicate that AA increases tonic adenosine modulation as a possible feedback loop to limit AA facilitation of neuronal excitability.

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