Fig. 3: HCN1 protein expression and Ih were significantly increased in dorsal CA1 region/neurons from susceptible group.

A, C Representative dorsal and ventral hippocampal slices immunolabeled with antibody against HCN1. Rectangle boxes depict the region of the slice used for quantification of the optical density. The arrows indicate increased perisomatic HCN1 protein expression. B, D Quantification of HCN1 protein expression from the perisomatic region to the distal dendritic region of CA1 from the dorsal and ventral hippocampi. E Western blot (top) and quantification (bottom) of HCN1 protein in dorsal CA1 region from the control, susceptible, and resilient groups. F, G We performed cell-attached voltage-clamp recordings. F Representative maximal h current traces in response to a 500-ms hyperpolarizing voltage step (−140 mV). G I_h was significantly increased in dorsal CA1 neurons from susceptible group compared with those from the control and resilient groups. H–L We performed whole-cell voltage-clamp recordings. H Representative current responses with step voltage commands ranging from −140 mV to − 60 mV (Δ = 10 mV) at a holding potential of −60 mV. The approximate position for determining the peak tail current is shown by black vertical dashed lines. I Susceptible group showed increased I_h in the dorsal CA1 neurons compared with those from the control and resilient groups. J The voltage dependence of activation for h channel was determined from tail currents (I_h / I_{h max}). The activation curve was fitted with a Boltzmann function with the following values: control V_1/2 = −101.8 mV, k = −14.13 mV, susceptible V_1/2 = −90.02 mV, k = −16.09 mV, resilient V_1/2 = −102.1 mV, k = −19.9 mV. K The half-activation voltage of h channel (V_1/2) for susceptible group was significantly shifted to the right by around +10 mV, whereas L the slope factor was not different between groups. Data are expressed as mean ± SEM.