Fig. 1.

Immunolabeling for neuropeptide Y (NPY) and β-secretase-1 (BACE1) increased in the hippocampal formation of epileptic mice. Low and high magnifications mid-hippocampal sections are from a control animal (Saline control) and pilocarpine-treated mice that developed status epilepticus and were sacrificed after surviving 2 days (2 d, post-status) or 2 months (Epileptic, 2 mo). Cell loss in areas CA3 and CA1 was seen in epileptic mice that survived 2 mo (C) as compared to control (A) or 2 d survival (B). Compared to control (D, G), NPY neoexpression in the mossy fiber terminals emerges at 2 d (E, H) but intensified with longer survival time (F, I). Mossy fiber sprouting into the inner molecular layer (indicated by triangles in “I”) was seen at the 2 mo survival time. NPY-labeled interneurons were seen in the cortex and hippocampal formation, including in the hilus (G). In control mice, BACE1 labeling in the control animal was prominent in the region of the mossy fiber pathway (J, M). The reactivity appeared to increase in the mossy fiber terminals from 2 d to 2 mo in the epileptic mice. Aberrant mossy fiber sprouting into the dentate inner molecular layer (indicated by triangles in “O”) was evident at the 2 mo survival point. Increased non-cellular labeling of BACE1 was also present in CA1 in 2 mo epileptic animals (L), with many darkly-labeled swollen terminals and processes present in the vicinity of the pyramidal cell layer (R, asterisks). DG: dentate gyrus; Hi:hilus; GCL: granule cell layer; s.p.: stratum pyramidale. Scale bar (in A)=1 mm for A–F and JL; bar=100 μm for G–I and M–R.