Figure 3.

DG excitability is increased in mice in which adult hippocampal neurogenesis is ablated. (A) Representative DCX immunostained coronal hippocampal sections of sham and x-irradiated mice. Total DCX counts: sham, 7873 ± 176.9, x-ray, 564.6 ± 148.9, Mean ± SEM, n = 3/gp, p < 0.0001. (B1–C1) (B1) and (C1) show time series data of VSD imaging of hippocampal circuit activity in response to electrical stimulation (100 μA, 1 ms) at DG with a bipolar extracellular stimulation electrode in sham and x-rayed mouse slices, respectively. (B2) and (C2) display the time courses of VSD signal [in the percent change of pixel intensity (ΔI/I%)] from the regions indicated by the small circles in the first frame in the DG center in (B1) and (C1), respectively. (D) Comparisons of the average peak strength of VSD response to electrical stimulation at center of DG of different amplitudes for the control and experimental groups. The data points (mean ± SE) are from 6 to 8 mice in each group (18–21 slices total), calculated for each slice and averaged for each animal. Because of slice conditions, responses for all stimulation intensities were not obtained from all slices. VSD response strength to DG electric stimulation (100 μA) differed significantly between sham and x-irradiated slices, p < 0.05. Analysis across all stimulation intensities showed a trend toward increased cellular activation in x-irradiated mice. Two-Way repeated measures ANOVA, (treatment) F_{(1, 11)} = 2.7, p = 0.12, (stimulation intensity × treatment) F_{(3, 33)} = 1, p = 0.4. (E) Total DG and CA3c activation (summed amplitudes of activated pixels across 10 peak response frames) in response to DG electric stimulation (100 μA) between sham and x-irradiated groups. ^*p <0.05.