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. 2006 Oct 2;103(41):15242–15247. doi: 10.1073/pnas.0602116103

Fig. 2.

Fig. 2.

Cell loss by apoptosis and no change in neurotransmitter phenotype. (A, B, and C) Coronal section at level of SN of P20 EnHT mouse stained against TH (green), activated caspase-3 (red), and DAPI (blue). The nigral DA neuron shows signs of apoptosis, a small rounded cell body, activated caspase-3, and a pyknotic nucleus (arrows). (D–H) Immunostaining against aromatic amino acid decarboxylase (Aadc) (D), Pbx1 (E), the En1-reporter β-Gal (G), and glutamate decarboxylase (Gad; H), and in situ hybridization against Ret (F), all on adult coronal brain sections of En2−/− (D–F, H), En1+/tLZ;En2−/− (EnHT) (D′–H′) and En1+/tLZ mice (G). Aadc, Pbx1, Ret, and β-Gal expression reveal all loss of nigral DA neurons in EnHT mice, whereas the Gad staining is the same in both genotypes (H). [Scale bars (A–C): 20 μm; (D–H): 500 μm.]

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