Figure 2.

The CA2 subfield was resistant to mesial temporal sclerosis-like neurodegeneration. A₁, A₂, A representative section from a control mouse stained for PCP4 (green) to label CA2 PNs and for Nissl (blue and white). Scale bar, 200 µm. B₁, B₂, CA2 PNs (STEP, green) are located adjacent to CA3a at the distal end of the mossy fiber projection in SL. Neuronal somata are visualized with a stain for Nissl (blue and white); labeling for NPY is shown in red. Scale bar, 100 µm. C₁, C₂, Representative mesial temporal sclerosis-like damage in a section from a PILO-SE mouse stained for PCP4 (green) and Nissl (blue and white). Scale bar, 200 µm. D₁, D₂, NPY expression in the mossy fibers was visible in all sections from PILO-SE mice. Neuronal somata (Nissl, blue and white) are absent from CA3a and are largely preserved in CA2 (STEP, green). Scale bar, 100 µm. E, Above, a heatmap showing the normalized fluorescence intensity of CA2-specific markers (see Materials and Methods) along the proximal–distal axis of stratum pyramidale in sections from control and PILO-SE mice. Below, normalized Nissl fluorescence intensity across CA3, CA2, and CA1 was decreased significantly in CA3, along with the proximal region of CA2 (CA2b) and the distal portions of CA1 (CA1b, CA1a; n = 45 sections from 31 control mice, n = 56 sections from 31 PILO-SE mice). F, Measurement of the mean normalized Nissl fluorescence in each subregion confirms a characteristic pattern of neurodegeneration in PILO-SE mice with mesial temporal sclerosis-like damage, in which CA2a and CA1c are relatively resilient to neurodegeneration.