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

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Fig. 2.
Fig. 2.

Brn3a regulatory sequences target gene expression only to primary sensory neurons, regardless of anatomical location. A cross-section of the midbrain of a newborn (P0) mouse stained for Brn3a by immunohistochemistry (A) and a vibratome section at a similar level stained for β-gal activity (B) show that β-gal expression controlled by Brn3a regulatory sequences is confined to primary sensory neurons of the mes5 (arrows) in the midbrain and not the numerous Brn3a-expressing tectal neurons. Comparison of Brn3a immunohistochemistry (C, E) and β-gal activity (D, F) in the P0 hindbrain shows that the nuclear expression of Brn3a protein in hindbrain reticular neurons and the inferior olivary nucleus is distinct from β-gal staining that corresponds to the projections of sensory axons to the trigeminal nucleus. In G, immunohistochemistry for β-gal protein shows expression of the LacZ transgene in a cervical dorsal root ganglion of a P0 mouse and in the associated proximal and distal roots. Aq, Aqueduct;Cb, cerebellum; d, distal root (of ganglion); DH, dorsal horn (of spinal cord);DRG, dorsal root ganglion; IC, principal nucleus of inferior colliculus; IO, inferior olive;mes5, mesencephalic trigeminal; p, proximal root (of ganglion); Pr5, principal trigeminal nucleus; pr5, principal tract of the trigeminal;Sp5, spinal trigeminal nucleus; SC, superior colliculus; VC, ventral cochlear nucleus.

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