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. Author manuscript; available in PMC: 2015 May 20.
Published in final edited form as: Neuroscience. 2013 Dec 4;259:214–222. doi: 10.1016/j.neuroscience.2013.11.054

Fig. 1.

Fig. 1

Experimental timeline and hippocampal neuronal loss in aged CaM/Tet-DTA mice. (A) Mice were aged for 12 months to allow for normal development. Doxycycline was removed from the diet to induce a 21-day lesion in the CA1 of the hippocampus. The mice were given 1 month for recovery after traumatic lesion, immediately followed by a 1-week twice-daily pulse of BrdU through IP injection. After injections, mice underwent a spatial memory-dependent behavioral task, Barnes maze, and were given a 1-week pulse of EdU 1 month from BrdU injections and sacrificed immediately after. (B) Light microscopic images of Nissl staining in hippocampal CA1 (B1 and B4), CA3 (B2 and B5), and DG (B3 and B6) subfield in non-lesioned (B1 and B3) and lesioned (B4 and B6) CaM/Tet-DTA mice at 14 months of age. (C) Stereological quantifications in the pyramidal layer of CA1 and CA3 and the granular cell layer of DG hippocampal subfield show a significant decrease in the cell number in lesioned (55.45% ± 2.20%, 22.38% ± 1.15%, and 51.48% ± 1.45%, respectively) compared to non-lesioned CaM/Tet-DTA mice. The values represent the mean ± SEM (n=6). **p<0.01, ***p<0.001. so, stratum oriens; sp, stratum pyramidale; sr, stratum radiatum. Scale bars=50 μm.