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. Author manuscript; available in PMC: 2010 May 1.
Published in final edited form as: Neurobiol Dis. 2009 May;34(2):308–319. doi: 10.1016/j.nbd.2009.02.001

Figure 8.

Figure 8

Early loss of thalamic relay neurons in Ppt1Δex4 knock-in mice. Histograms of unbiased optical fractionator estimates of the number of Nissl stained lamina IV granule neurons and lamina V projection neurons in somatosensory barrelfield (S1BF) cortex; the ventral posterior nucleus of the thalamus (VPM/VPL), which provides afferent input to S1BF; and visual relay neurons in the dorsal lateral geniculate thalamic nucleus (LGNd) of Ppt1Δex4 mice and age-matched controls (+/+) at different stages of disease progression. No significant loss of cortical neurons in laminae IV or V of S1BF was evident in Ppt1Δex4 mice at either 1 or 4 months of age. In marked contrast, and consistent with the phenotype of Ppt1-/- mice (Kielar et al., 2007), a significant loss of both VPM/VPL and LGNd neurons was already observed at 4 months of age. (* p<0.05; *** p<0.001, ANOVA with post-hoc Bonferroni analysis).