Brain-derived neurotrophic factor-, neurotrophin-3-, and tyrosine kinase receptor-like immunoreactivity in lingual taste bud fields of mature hamster after sensory denervation

Unlike lingual taste buds in most mammals, fungiform buds on the anterior tongue of mature hamster survive sensory denervation. The role of the neurotrophin ligands, brain‐derived neurotrophic factor (BDNF) and neurotrophin‐3 (NT‐3), and their respective tyrosine kinase (Trk) receptors, TrkB and TrkC, in denervated taste buds is not known. The present report investigates changes in the degree of gemmal cell immunoreactivity (IR) (i.e., number of immunoreactive cells/bud profile) and density of nerve fiber‐IR of these markers in unilaterally denervated mature hamsters. The fungiform bud field after chorda tympani/lingual nerve resection is compared with the nerve‐dependent, posterior tongue foliate and circumvallate bud fields after glossopharyngeal nerve resection. Four weeks post lesion, the number of denervated fungiform buds matched that on the unoperated side, whereas denervated foliate and circumvallate bud counts decreased by 72% and 38%, respectively. In taste buds that survived on the posterior tongue, the degree of foliate bud cell BDNF‐, NT‐3‐, and TrkB‐like IR, and circumvallate bud cell BDNF‐ and NT‐3‐like IR, significantly decreased compared with the unoperated side. In contrast, for anterior tongue fungiform bud cells, the degree of neurotrophin‐ and receptor‐like IR was relatively less affected: NT‐3‐ and TrkB‐like IR were unchanged; BDNF‐like IR, although significantly decreased, was also maintained. Moreover, TrkB‐like fiber IR was essentially eliminated within and surrounding fungiform buds. Hence, NT‐3‐, BDNF‐, and TrkB‐like IR in fungiform gemmal cells may reflect an autocrine capacity promoting survival. Because TrkC‐like IR in bud cells is absent (i.e., immunonegative), and sparse in fibers intragemmally and perigemmally, NT‐3 may also bind to bud cell TrkB so as to sustain fungiform gemmal cell viability post denervation. J. Comp. Neurol. 455:25–39, 2003. © 2002 Wiley‐Liss, Inc.