Abstract
Brain-derived neurotrophic factor (BDNF) and neurotrophin-4 (NT-4) are two neurotrophins that play distinct roles in geniculate (taste) neuron survival, target innervation, and taste bud formation. These two neurotrophins both activate the tropomyosin-related kinase B (TrkB) receptor and the pan-neurotrophin receptor p75. Although the roles of these neurotrophins have been well studied, the degree to which BDNF and NT-4 act via TrkB to regulate taste development in vivo remains unclear. In this study, we compared taste development in TrkB−/− and Bdnf−/−/Ntf4−/− mice to determine if these deficits were similar. If so, this would indicate that the functions of both BDNF and NT-4 can be accounted for by TrkB-signaling. We found that TrkB−/− and Bdnf−/−/Ntf4−/− mice lose a similar number of geniculate neurons by E13.5, which indicates that both BDNF and NT-4 act primarily via TrkB to regulate geniculate neuron survival. Surprisingly, the few geniculate neurons that remain in TrkB−/− mice are more successful at innervating the tongue and taste buds compared with those neurons that remain in Bdnf−/−/Ntf4−/− mice. The remaining neurons in TrkB−/− mice support a significant number of taste buds. In addition, these remaining neurons do not express the TrkB receptor, which indicates that either BDNF or NT-4 must act via additional receptors to influence tongue innervation and/or targeting.
Highlights
The cell bodies of taste neurons are located in the geniculate ganglion
To understand whether the regulation of geniculate neuron loss by these two neurotrophins acts via the same receptor, tropomyosin-related kinase B (TrkB), we quantified the number of geniculate neurons in wildtype, Bdnf2/2/Ntf42/2, and TrkB2/2 mice from E11.5 to E13.5
We reasoned that if TrkB mediates the effects of these two ligands, Bdnf2/2/Ntf42/2 and TrkB2/2 mice would lose a similar number of geniculate neurons over the same timeframe
Summary
The cell bodies of taste neurons are located in the geniculate ganglion. During development, taste neurons innervate specific regions of the gustatory epithelium with a precise number of neurons. The development of the geniculate ganglion and the formation of peripheral connections are highly regulated by two neurotrophins, brain-derived neurotrophic factor (BDNF) and Neurotrophin-4 (NT-4). Bdnf2/2 and Ntf42/2 mice each lose approximately 50% of their geniculate neurons by birth [1,2]. NT-4 regulates the survival of geniculate neurons at an earlier stage of development compared with BDNF via a different mechanism [3]. BDNF in the tongue epithelium directs gustatory axons to their correct targets, while NT-4 does not [4,5]. Bdnf2/2 mice, which have a deficit in targeting, have a more severe loss of innervation to taste buds than Ntf42/2 mice [3,6,7,8]
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