Taste neurons consist of both a large TrkB-receptor-dependent and a small TrkB-receptor-independent subpopulation.

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.