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. 2012 Feb 22;107(10):2769–2781. doi: 10.1152/jn.00528.2011

Fig. 3.

Fig. 3.

Adenosine inhibits the evoked glutamatergic input to MCPO/SI cholinergic neurons through presynaptic A1 receptors. A: adenosine (100 μM) inhibits glutamatergic AMPA-receptor-mediated evoked excitatory postsynaptic currents (evEPSCs); 2,3-dioxo-6-nitro-1,2,3,4-tetrahydrobenzo[f]quinoxaline-7-sulfonamide (NBQX) was used at 10 μM. AD, adenosine. B: adenosine increases paired-pulse facilitation (PPF; paired-pulses test using 40-ms interstimulus interval). At right, scaled traces to match evEPSC (1st pulses) are represented to show the increased PPF by adenosine. C and D: adenosine inhibition of evEPSCs is blocked by the A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 100 nM) and is mimicked by the A1 agonist N6-cyclopentyladenosine (CPA; 100 nM). E–G: evoked glutamatergic EPSCs are unaffected by the A2A receptor agonist CGS-216800 (0.1–3 μM), the A2 receptor agonist CV-1808 (250 nM), or the A3 receptor agonist Cl-IB-MECA (100 nM). H and I: DPCPX (100 nM) increases the amplitude of evEPSCs by blocking endogenous adenosine. J: summary graph showing the averaged effects of adenosine, adenosine in the presence of DPCPX, CPA, CPA in the presence of DPCPX, CGS-21680 (0.1 and 3 μM), CV-1808, Cl-IB-MECA, and DPCPX on evEPSC amplitude. *P < 0.05;**P < 0.01, paired t-test, comparing evEPSC amplitude in control artificial cerebrospinal fluid (ACSF) and during drug applications. All evEPSCs were recorded at Vh = −70 mV.