Guimas Almeida, ClaudiaDe Mendonça, AlexandreCunha, Rodrigo A.Ribeiro, Joaquim A.2022-12-152022-12-152003Neurosci Lett. 2003 Mar 20;339(2):127-1300304-3940http://hdl.handle.net/10451/55413© 2003 Elsevier Science Ireland Ltd. All rights reserved.Reactive oxygen species (ROS) are believed to be involved in the pathogenesis of several neurological disorders. We now tested whether the endogenous neuroprotective substance, adenosine, attenuates the cell damage induced by ROS. In rat hippocampal slices, the xanthine oxidase (40 mU/ml) plus xanthine (1 mM) (X/XO) system produced a 27.8+/-7.3% (n=3) increase in ROS, measured by fluorimetry with 2',7'-dichlorodihydrofluorescein, a 246.9+/-18.4% (n=6) increase in the release of tritiated adenosine, and a decrease in synaptic transmission that fully recovered after washout. In the presence of the adenosine A(1) receptor selective antagonist, 1,3-dipropyl-8-cyclopentylxanthine (100 nM), X/XO induced a similar inhibition, however synaptic transmission only recovered to 70.7+/-5.8% of control (n=5). The blockade of A(2A) receptors was devoid of effect (n=4). Adenosine is released by ROS-generating systems, and attenuates the deleterious cellular consequences of ROS through A(1) receptor activation.engAdenosineNeuroprotectionReactive oxygen speciesHippocampusA1 receptorsA2A receptorsDipropylcyclopentylxanthinejournal article10.1016/S0304-3940(02)01478-71872-7972