Deficiency in IFNGR signaling prevents perisomatic bouton loss in DCN and affords partial protection against dendritic alterations in spinal cord. Viral déjà vu experiments were conducted with bone marrow chimeric carrier mice of the indicated genotypes and carrier state. At the peak of disease (day 10) synaptophysin⁺ perisomatic boutons on DCN neurons (A and B) and MAP-2⁺ dendritic processes into the spinal cord white matter (C and D) were visualized by immunohistochemistry. (A) Representative picture of synaptophysin⁺ boutons in DCN of the various experimental groups. Arrowheads indicate perisomatic boutons of WT→WT noncarrier control animals and on neurons of WT→IFNGR^−/− mice. (B) Quantitative analysis of perisomatic bouton density in the same animals as in A. Error bars indicate the mean + SEM of 3–7 mice per group. (C) Representative pictures of spinal cord MAP-2 staining in the indicated groups. (D) Dendritic projections into the spinal cord white matter in WT→IFNGR^−/− and WT→WT areas were quantified on MAP-2–immunostained sections. Error bars represent the mean + SEM of three to six mice per group. Bars: (A) 10 µm; (C) 50 µm. Shown are representative data from one out of two similar experiments (A–D). *, P < 0.05; **, P < 0.01.