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. 2004 Mar 24;24(12):2942–2952. doi: 10.1523/JNEUROSCI.0092-04.2004

Figure 2.

Figure 2.

Correlation of [3H]compound D binding sites and PS-1 gene expression in mouse embryos. A–C, Representative parasagittal sections from wild-type (PS-1+/+), heterozygous (PS-1+/–), and homozygous (PS-1–/–) PS-1 knock-out embryos (n = 4 for each genotype). Note the global reduction of binding sites in the heterozygous (B) and homozygous (C) relative to the wild type (A). D, Level of nonspecific binding as a control for these embryo sections. E, Quantification of binding densities measured from the dorsal wall of the telencephalic vesicle (telencephalon), the liver, and the wall of the rudimentary gastrointestinal duct (GI). The readings of binding density of the same region were normalized to those from the wild-type embryos. Note that there are ∼50 and 80% losses of binding sites in the PS-1+/– and PS-1–/– embryos, respectively, relative to the wild type in the representative central and peripheral regions. F, Representative gel analysis of the PCR product of the three genotypes of embryos. The products of the wild-type (WT) allele and the PS-1–/– allele are ∼500 and 250 bp, respectively, whereas those for PS-1+/– allele contain both. The broken line approximately outlines the border of the brain and spinal cord (SC). LV, Lateral ventricle; 4V, fourth ventricle. Scale bar, 250 μm.