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Fig. 3 | Acta Neuropathologica Communications

Fig. 3

From: Insulin-like growth factor-1 overexpression increases long-term survival of posttrauma-born hippocampal neurons while inhibiting ectopic migration following traumatic brain injury

Fig. 3

IGF1 decreases ectopic localization of new neurons within the dentate gyrus after injury. (a) Posttrauma-born mature neurons immunolabeled for Neuronal Nuclei (NeuN, green) and the proliferation reporter bromodeoxyuridine (BrdU, red) primarily localized to the inner granule cell layer (iGCL) and the outer 2/3rd region of the granule cell layer (oGCL, white arrows) after controlled cortical impact (CCI). S, subgranular zone. (b) Mature neurons (NeuN+BrdU+) were occasionally observed in the hilar layer (HL) and the molecular layer (ML) after CCI. White arrows highlight double-labelled cells; the scale bar represents 10 μm. IGF1 overexpression was associated with a significant increase in the density (cells/mm3) of matured post-trauma proliferated neurons in both the iGCL (c) and oGCL (d) at 6 weeks after brain injury. (e) The proportion of proliferated GCL neurons that localized to the oGCL was increased by IGF1 overexpression. (f) Brain injury stimulated the ectopic migration of a small subset of new neurons into the ML and HL in both injured WT and injured IGFtg mice. The ML and HL NeuN+BrdU+ densities (cells/mm3) are separated for illustrative purposes. (g) However, the proportion of acutely born neurons that matured and localized ectopically to the ML or HL was reduced by IGF1 overexpression. Data presented as mean + SEM; Sham n = 3/genotype, CCI n = 8–9/genotype; One-way ANOVA, followed by Bonferroni’s selected comparisons post-hoc t-tests. *p < 0.05 and **p < 0.01 compared to sham controls. &p < 0.05 and &&p < 0.01 compared to injured WT

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