The Death Receptor Antagonist FLIP-L Interacts with Trk and Is Necessary for Neurite Outgrowth Induced by Neurotrophins

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Figure 2.
Figure 2.

Distribution of FLIP-immunoreactive cells during the development of mice brain. A–C, In the cerebral cortex, many cells show immunohistochemical labeling. A, E16 neurons contain FLIP in the cortical plate (CP) and subplate (SP). B, At P5, some neurons in layers II–III present weak immunostaining (arrows); in contrast, at this age, some cells located throughout all cortical layers are FLIP immunopositive (arrowheads). C, At P15, FLIP-positive cells present in all cortical layers show an astrocytic morphology. D–F, In the cerebellum, the soma of some Purkinje cells shows immunohistochemical staining at embryonic (arrows in D) and early postnatal mice (arrows in E). At later postnatal stages, cells located just under the Purkinje cell layer and scattered in the granule cell layer show FLIP immunostaining (F). G–I, Immunofluorescence colocalization (arrows) of FLIP and NeuN (specific neuronal marker) in cortical plate at E16. J–L, Double immunostaining with antibodies detecting FLIP and GFAP in cerebral cortex at P15 showed the expression of FLIP in some GFAP-positive astrocytes (arrows). MZ, Marginal zone; IZ, intermediate zone; VZ, ventricular zone; ML, molecular layer; PCL, Purkinje cell layer; GL, granule cell layer. Scale bars: (in C) B–F, 100 μm; (in J), G–L, 50 μm.

  1. The Journal of Neuroscience vol. 30 no. 17 6094-6105
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