Neural cell adhesion molecule, neuron-specific enolase and calcitonin gene-related peptide immunoreactivity in hamster taste buds after chorda tympani/lingual nerve denervation.

Hamster fungiform papilla taste buds persist in an atrophic form following sensory denervation. While atrophic and innervated taste buds are morphologically similar, it is not known whether their gemmal cells have similar molecular characteristics. Three neurochemicals, neural cell adhesion molecule, neuron-specific enolase, and calcitonin gene-related peptide have been implicated in trophic phenomena, synaptogenesis and cell recognition in neurons and sensory neuroepithelia. The present study uses immunocytochemical localization of these molecular markers to characterize normal and denervated fungiform taste buds following unilateral chorda tympani/lingual nerve denervation in hamsters. In normal taste buds, immunoreactivity to neural cell adhesion molecule, neuron-specific enolase, and calcitonin gene-related peptide was present in a group of cells located centrally in the bud as well as in fungiform nerve fibres and endings. After denervation, gemmal cell immunoreactivity to all three markers was reduced and often confined to a single or a few bud cell(s). Also, fibre staining was absent except for sparse calcitonin gene-related peptide-immunoreactive fibres associated with blood vessels and within the fungiform papillae. These remaining fibres may be autonomic or somatomotor in origin. These results indicate that sensory denervation of hamster taste buds reduces, but does not wholly eliminate the immunoreactivity of surviving gemmal cells to neural cell adhesion molecule, neuron-specific enolase, and calcitonin gene-related peptide. While the number of taste bud cells expressing the markers appears to be nerve-dependent, immunoreactivity in sensory-denervated bud cells of hamster may reflect the influence of local tissue factors.