Defects in Sensory Axon Growth Precede Neuronal Death in Brn3a-Deficient Mice

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Fig. 5.
Fig. 5.

Sensory neuronal death in late gestation in Brn3a null mice. Brn3a+/− (A,C) and Brn3a−/− (B,D) embryos were examined by β-gal activity staining at E16.5, after the onset of sensory neural apoptosis. Although the sensory ganglia can no longer be seen in the Brn3a−/− embryo, β-gal activity persists in the sensory axons, and numerous defects in axonal guidance can be seen in the mutant embryos (B). The defect in the encirclement of the whisker follicles noted at E13.5 also persists at this stage (D).

  1. The Journal of Neuroscience vol. 21 no. 2 541-549
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