Fig. 1

Effects of FK506 on markers of neurodegeneration in gp120 tg mice. Non-tg and gp120 tg mice were treated with vehicle or FK506 for 4 weeks, and immunostained serial vibratome sections were analyzed by digital bright-field microscopy and confocal microscopy. Representative images are shown from the frontal cortex. a Representative bright-field microscopic images and b computer-aided ImageJ analysis of sections incubated with an antibody against the neuronal marker NeuN showing decreased immunoreactivity in the neocortex in vehicle-treated gp120 tg mice. In vehicle-treated gp120 tg mice, there was a significant decrease (*p < 0.05, by one-way ANOVA post hoc Dunnett’s), while FK506 treatment ameliorated the neuronal alterations compared to vehicle-treated gp120 tg mice (^# p < 0.05, by one-way ANOVA post hoc Tukey-Kramer). c Immunocytochemical analysis and confocal microscopy of sections labeled with an antibody against the dendritic marker MAP2 (FITC channel). d Computer-aided ImageJ analysis of the % area of the neuropil that is MAP2 immunostained. In vehicle-treated gp120 tg mice, there was a significant decrease in MAP2 immunoreactivity. e Immunofluorescent microscopy and f image analysis of the synaptic marker synaptophysin revealed a statistically significant synaptic loss in vehicle-treated gp120 mice compared to vehicle-treated non-tg mice, and treatment with FK506 rescued the synaptic loss in gp120 mice. Scale bar = 20 μm. *p value <0.05 by one-way ANOVA and Dunnett’s post hoc analysis compared to vehicle; N = 10; age = 12 months of age