Fig. 2

Contribution of glutamatergic activity to VSD and IOS transients. a: (Left) Representative VSD amplitude maps under control condition and 100 μM APV + 20 μM CNQX application. (Right) Effect of 100 μM APV + 20 μM CNQX application on the population spike (PS) measured in the CA1 and on the average VSD and IOS amplitudes in the CA1, CA3 and DG regions. b: (Left) Representative IOS and VSD amplitude maps under control condition and 300 μM DHK application. (Middle) Time course of the field potential responses and VSD transients on the diode at the field potential recording site under control conditions and during 300 μM DHK application. (Right) Effect of 300 μM DHK on the PS measured in the CA1 and on the average VSD and IOS amplitudes in the CA1, CA3 and DG regions. c: (Left) Distribution of inhibitory effect of 100 μM APV + 20 μM CNQX application on the VSD amplitude of each diodes in % of control. The valley between the two peaks on the histogram is marked by an arrow. (Middle) Representative VSD inhibition map during 100 μM APV + 20 μM CNQX + 300 μM DHK application in % of control. Area identified as monosynaptically activated is contoured by white line. (Right) Effect of 100 μM APV + 20 μM CNQX + 300 μM DHK on the PS measured in the CA1 and on the average VSD amplitude in the monosynaptically activated area. On the optical signal amplitude maps transparent lines indicate the pyramidal cell layers (CA1 and CA3) and the granular cell layer of the DG. The positions of the stimulating and recording electrodes are marked by gray and green arrows, respectively. Asterisks indicate significant changes compared to control (P < 0.05, Mann–Whitney U test)