Fig. 2. Brn3a regulates sensory neurotransmitter systems. The cranial sensory ganglia of control (Brn3a^+/+) and knockout (Brn3a^–/–) E13.5 embryos were examined for the expression of components of neurotransmitter systems. (A) The plane of section used in subsequent views is illustrated using an E13.5 embryo stained for the expression of ß-galactosidase regulated by a Brn3a sensory enhancer (Eng et al., 2001). (B) In situ hybridization showing the expression of the Brn3a mRNA in the cranial sensory ganglia. (C) In situ hybridization for the 5HT3 receptor, increased in the microarray analysis of Brn3a knockout mice, and the mediator of G-protein signaling RGS10, decreased in the microarray. (D-F) Immunohistochemistry for the products of Brn3a target genes in the trigeminal ganglia of E13.5 embryos. (D) Galanin immunoreactivity in the trigeminal ganglion co-localized with Brn3a in a majority of trigeminal neurons. (E) Tyrosine hydroxylase was expressed in a more limited subset of trigeminal neurons, most of which also expresses Brn3a. (F) A comparison of trigeminal ganglia from control mice and Brn3a knockouts, showing that, as predicted from the microarray studies, calretinin (Calret) and somatostatin (Som) immunoreactivity is markedly increased in the absence of Brn3a, whilst galanin is reduced to below the threshold of detection, and tyrosine hydroxylase (TH) is also significantly decreased. 5g, trigeminal ganglion; 8g, vestibulocochlear ganglion; 9g, IX/X ganglion complex; di, diencephalon; drg, dorsal root ganglion; hb, hindbrain; ot, otic region; tel, telencephalon; sc, spinal cord. Scale bars: B, 400 µm, D,E, 25 µm; F, 200 µm.