Fig. 5

Mild bTBI caused axonal injury in the hippocampus. Mild blast exposure did not result in macroscopic damage, but induced microscopic pathological effects, such as axonal damage and neuroinflammation in the hippocampus. a Absence of macroscopic hippocampal tissue damage at 7 days post-bTBI as tested in anterior-posterior 4 mm coronal rat brain sections. b Absence of overt neuronal injury in hippocampus at 7 days post-bTBI as assessed with H&E staining. Insert shows no overt pathology in the CA3 hippocampal subfield. c Absence of Fluoro-Jade B-positive neurons in the hippocampus at 7 days post-bTBI. Insert shows no degenerating neurons in CA3. d and e Increased phosphorylated neurofilament immunostaining in CA3 at 3 days post-bTBI (e) compared to control subjects (d). f Bar graph of normalized signal of phospho-specific anti-neurofilament antibody, SMI-31, staining in hippocampal area CA3 from controls and rats at 3 days post-bTBI is shown. Signal was quantitated on n = 9–12 slides from 3 individual rats for each treatment group (3–4 slides/rat). Data are presented as mean ± SEM; *p < 0.05; Student’s t-test. g Swollen dystrophic axon in hippocampal CA1 stratum pyramidale at 3 days post-blast are indicated by arrowhead. h Axonal bulb in the hippocampal hilus at 7 days post-bTBI is indicated by arrowhead. Representative microscope pictures of hippocampal sub-regions immunostained with SMI-31 antibody (d, e, g, and h). Scale bars: 50 μm (b-e); 20 μm (g and h)