7-(2-phenylethyl)-5-amino-2-(2-furyl)-pyrazolo-[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine (SCH58261; a selective A2AR antagonist; Tocris, USA) and 2-p-(2-carboxyethyl)phenethylamino-5′-N-ethylcarboxamidoadenosine (CGS21680; a selective A2AR agonist; Tocris, USA) were dissolved in saline containing 10% dimethylsulfoxide (DMSO) and administered systemically by intraperitoneal (i.p.) injection at the doses of 0.1 and 0.2 mg/kg, respectively (in a volume of 1 mL/kg) immediately after the fear conditioning session, unless otherwise specified. The doses and concentrations used in this study were chosen based on previous studies (see [11 (link), 15 (link), 21 (link)]). For the electrophysiological experiments testing the modification of adenosine A1 receptor (A1R) function, we used the closest but stable chemical analog of adenosine, 2-chloroadenosine (CADO, from Sigma-Aldrich, Portugal) in a previously validated concentration range of 0.1–1 μM [22 (link)] as well as the selective A1R antagonist, 1,3-dipropylcyclopentlxanthine (DPCPX, from Tocris), used in a supra-maximal and selective concentration of 100 nM [23 (link)]. It should be noted that although CADO can activate A1R and A2AR, the fact that A2AR are devoid of effects in the control of basal synaptic transmission [24 (link), 25 (link)], allows using CADO to selectively probe the efficiency of A1R to control hippocampal synaptic transmission [22 (link), 23 (link)].
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