Figure Legends
Figure. 1. MRS5474 did not affect excitatory postsynaptic currents (EPSCs) in CA1 pyramidal cells at hippocampal slices . Time-course changes of EPSC peak amplitude are shown inA (n=6 cells, from 5 animals), B (n=5 cells, from 4 animals; QX-314 in the intracellular solution to inhibit sodium channels and prevent action potential spiking independently of input strength) and C (n=5 cells, from 4 animals). EPSC peak amplitude was normalized in each experiment taking as 100% baseline the values recorded for 10 minutes before drug application (1); drug effects were assessed by comparing baseline values with values recorded at 30–40 minutes after drug application (2). Values are as mean \(\pm\) SEM. The horizontal lines below drug names indicate drug presence in the perfusion solution. Insets in each panel: representative averaged superimposed EPSC traces recorded in the same cell before (1) and by the end (2) of drug application. In B are shown paired EPSC amplitude (pA) of all cells in A , in baseline (period 1 indicated in A ) and under MRS5474 (period 2 indicatedA ; ns: P>0.05, two tailed paired t-test). In all experiments, the fast component of inhibitory GABAergic transmission was blocked by adding picrotoxin (50 μM) to the aCSF. Note that the selective A1R agonist, CCPA (C ) caused a marked inhibition of EPCs in clear contrast to the absence of effect of MRS5474 (A, B ).
Figure 2. MRS5474 did not affect field excitatory post synaptic potentials (fEPSPs) in hippocampal slices in control conditions, in clear contrast with the A1R agonist, CPA. In panels A andB are shown normalized averaged time-course changes in fEPSP slopes (%, mean \(\pm\) SEM) taking as baseline (100%) the values recorded for 10 minutes before drug application. The horizontal lines below drug names indicate drug presence in the perfusion solution and the arrows indicate the time of starting perfusion of each drug concentration. Insets: representative superimposed averaged fEPSPs traces recorded from the same slice before (control) and by the end of (A ) MRS5474 (250nM) or (B ) CPA (30 nM) application.A : n=7 slices from 6 animals. B : n=4 slices from 4 animals. Note that the selective A1R agonist, CPA (B ) caused a marked inhibition of fEPSPs in clear contrast to the absence of effect of MRS5474 (A ).