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

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Fig. 6.
Fig. 6.

Sensory axon guidance in TrkC neurotrophin receptor-deficient mouse embryos. Mice carrying the 11 kb/LacZ transgene were interbred with TrkC+/− mice, and then the resulting 11 kb/LacZ, TrkC+/− mice were crossed with TrkC+/− mice to produce litters containing the 11 kb/LacZ, TrkC+/− embryos (A, C) and 11 kb/LacZ, TrkC−/− (B, D) littermates. Examined at E13.5, TrkC mutant embryos lack the ectopic trigeminal branches noted in Brn3a null mice (A,B) and show normal encirclement of the whisker follicles by β-gal-expressing sensory axons (C,D). 5g, Trigeminal ganglion;Mn, mandibular division, trigeminal nerve;Mx, maxillary division, trigeminal nerve;Op, ophthalmic division, trigeminal nerve;Pr5, principal trigeminal nucleus.

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