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. 2011 Sep;85(17):8528–8537. doi: 10.1128/JVI.00809-11

Fig. 3.

Fig. 3.

Neuropathology in infected prairie voles and Tg1536 mice. Hematoxylin- and eosin-stained hippocampal and cerebellar sections from terminal CWD (Positive) and sham-inoculated (Sham) Tg(CerPrP)1536 mice (A to D) and voles (E to L). (A to D) Neuropil spongiosis and plaque formation (arrow) were observed only in the hippocampi of CWD-inoculated Tg(CerPrP)1536 mice (A) but not sham-inoculated animals (B). No degeneration was seen in the cerebellum of CWD-infected (C) or sham-inoculated (D) Tg(CerPrP)1536 mice. (E to H) Prairie voles (CWD-voles) inoculated with CWD-infected deer brain D10 (Positive) or with negative deer brain (Sham). Significant neurodegeneration was not identified in hippocampal or cerebellar sections. (I to L) Prairie voles (vPMCA-voles) inoculated with vPMCA product generated by PMCA (Positive) or with NBH from PMCA (Sham). No degeneration was seen in the hippocampus of infected (I) or sham-inoculated (J) voles. Marked loss of granular cell neurons and Purkinje cells (arrow) was noted in the cerebellar cortex of infected vPMCA-voles (K) but not sham-inoculated voles (L). Scale bars, 500 μm (A to G, I, K, and L), 150 μm (H), and 300 μm (J).