Fig. 1. Characterization of the cells that express the H-2Z1 transgene in the cerebral cortex: A–G, β-galactosidase activity is visualized as a blue(A, C, F–K) or a fluorescence (white in D,E) reaction product. A, Whole-mount staining of the right telencephalic hemisphere of a P8 H-2Z1 mouse oriented to provide an upright position to the somatotopic body representation disclosed by transgene expression, which is schematized in B [modified from Dawson and Killakey (1987)]. Thein situ orientation is given by thearrows. d, Dorsal; a, anterior. The asterisks mark additional staining, probably located in the secondary somatosensory area. C, Sagittal section of a P8 brain illustrating the layer-specific expression of the H-2Z1 transgene; the arrowhead marks a deep neuron that expresses β-galactosidase. D,E, The diffusible substrate FDG fills the cell bodies of H-2Z1-positive cells; the arrowheadsdelineate a single barrel in D and labeled neurites inE. F, G, β-galactosidase activity is localized to small vesicles in the cell body (arrow in F) that accumulate in one to three locations in the cytoplasm (arrowhead inF) and seem to mark some axons (arrowheads in G). H–J, Transverse sections through the somatosensory area of young adult mice treated by double-labeling for the detection of H-2Z1 expression (inblue, arrowheads inH–K) and GAD 67 (purple,arrow in H), calretinin (brown, arrow inI), parvalbumin (brown,arrow in J), or calbindin (brown, arrow inK). H-2Z1 was never colocalized with GAD 67, calretinin, or parvalbumin. In contrast, some H-2Z1-positive cells coexpressed calbindin. Scale bar (shown in F):A, 400 μm; C, 1 mm; D, 100 μm; E, H, 35 μm; G,K, 20 μm; I, J, 50 μm.