3.8 Article

Histochemical changes and apoptosis in degenerating taste buds of the rat circumvallate papilla

Journal

ARCHIVES OF HISTOLOGY AND CYTOLOGY
Volume 72, Issue 2, Pages 91-100

Publisher

INT SOC HISTOLOGY & CYTOLOGY
DOI: 10.1679/aohc.72.91

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Funding

  1. Ministry of Education, Culture, Science, Sports and Technology of Japan
  2. Japan Society for the Promotion of Science [19390464]
  3. Grants-in-Aid for Scientific Research [19390464] Funding Source: KAKEN

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The present study was designed to examine the histochemical changes and occurrence of apoptosis in taste buds of rat circumvallate papillae following bilateral transection of the glossopharyngeal nerve. Following transection of the glossopharyngeal nerve, the number of taste buds was not altered until postoperative day 3 (PO3), but decreased significantly thereafter. The number of cells within a taste bud, however, decreased significantly from PO2. In normal, uninjured animals, approximately 15.4%, 9.0%, and 7.7% of taste bud cells were labeled with antibodies for phospholipase C beta 2 subunit (PLC beta 2), a marker for type II cells, neural cell adhesion molecule (NCAM), a marker for type III cells, and Jacalin, a marker for type IV cells, respectively. Following gustatory nerve injury, the ratio of cells expressing markers of type III and type IV decreased gradually from PO2, and Jacalin-labeled taste bud cells disappeared on PO3. Under normal conditions, immunoreactivity for single-strand DNA (ssDNA), a marker of apoptosis, was detected in the nuclei of PLC beta 2-immunoreactive cells and cells showing no labeling for PLC beta 2, NCAM, or Jacalin. On PO1, the number of taste bud cells showing ssDNA immunoreactivity increased to double that of normal uninjured animals; these ssDNA-immunoreactive cells were also labeled with NCAM and Jacalin as well as PLC beta 2. The present results suggest that denervation of the gustatory nerve causes apoptosis in all types of taste bud cells, resulting in the rapid degeneration of taste buds.

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