Fig. 7.
dCA2 inputs recruit more disynaptic inhibition in vCA1a than in deep dCA1. AAV-DIO-ChR2-eYFP was injected in dCA2 of Amigo2-Cre mice. a Synaptic input-output curves following photostimulation of dCA2 inputs at indicated intensities in deep dCA1 PNs, before and after blockade of GABAA receptors with 2 µM SR 95531 and GABAB receptors with 1 µM CGP 55845. 100% light intensity defined in Fig. 6 legend. Blockade of inhibition caused a small, statistically non-significant increase in the peak PSP (n = 7 cells, 3 mice; two-way ANOVA: treatment × light intensity F(10,132) = 0.06631, P > 0.9999; treatment F(1,132) = 1,741, P = 0.1893). b Input-output curves following photostimulation of dCA2 inputs to vCA1a PNs, before and after 2 µM SR 95531 and 1 µM CGP 55845. Blockade of inhibition blockade produced a significant ~twofold increase in the PSP amplitude (n = 9 cells, 5 mice; two-way ANOVA: treatment × light intensity F(10,154) = 0.4744, P = 0.9046; treatment F(1,154) = 17.79, P < 0.0001). c Ratio of the peak PSP after inhibition block divided by PSP before inhibition block is greater in vCA1a than in deep dCA1 (two-way ANOVA: dorsal/ventral × light intensity F(9,129) = 0.2679, P = 0.9821; dorsal/ventral F(1,129) = 23.06, P < 0.0001). Results show mean ± s.e.m.****P < 0.0001; ns, P > 0.05