FGF-2 regulates neurogenesis and degeneration in the dentate gyrus after traumatic brain injury in mice
J. Clin. Invest. Shinichi Yoshimura, et al. 112:1202 doi:10.1172/JCI16618 [Go to this article.]

Figure 4
Cell loss in ipsilateral GCL of DG after CCI in FGF-2^+/+ and FGF-2^–/– mice. (a) Mice were killed on either day 9 or day 35 after CCI. Coronal brain sections were obtained at bregma –2.5 mm (cresyl violet staining). In sham-operated animals, there were no differences in DG morphology between FGF-2^+/+ and FGF-2^–/–, and no apparent cell loss was observed at 35 days (upper panels). By 9 days after CCI, cell loss was apparent in the superomedial part of the upper blade of the DG in both FGF-2^+/+ and FGF-2^–/– mice (arrowheads, middle panels). By 35 days, cell loss was more prominent in FGF-2^–/– mice (arrowheads, lower panels). Scale bar: 100 μm. Changes in volume (b) and cell loss (c) in GCL of DG after CCI in FGF-2^+/+ and FGF-2^–/– mice. Mice were killed at either 9 or 35 days after CCI, and coronal brain sections were stained with cresyl violet. The GCL volume in the ipsilateral DG was expressed as a percentage of volume measured in the corresponding region within the contralateral DG (see Methods). The percentage change in the number of neurons within GCL in the ipsilateral DG was calculated relative to that of the contralateral side (see Methods). GCL volume and neuron numbers were significantly decreased in FGF-2^–/– mice (white bars) compared with FGF-2^+/+ mice (black bars) 35 days after injury. ^†P < 0.05 compared with mice of same genotype 9 days after CCI. *P < 0.05 compared with FGF-2^+/+ mice on the same day after injury (n = 4–7 per group).