Morphology of taste buds in the circumvallate papilla from mutant dystonia (dt/dt) mice and diabetic (db/db) mice

• Main Authors: Yu-Jen Su, 蘇昱人
• Other Authors: 盧國賢
• Format: Others
• Language: zh-TW
• Published: 2007
• Online Access: http://ndltd.ncl.edu.tw/handle/17498510447690507071

碩士 === 國立臺灣大學 === 解剖學暨生物細胞學研究所 === 95 === Recently studies on the taste bud are focused on the neurotransmitters and cell communications and seldom the morphology, of the taste bud. Dystonia musculorum (dt) was originally described as a hereditary sensory neurodegeneration syndrome of the mouse (mutant dt/dt). The gene defective in dt encodes a cytoskeletal linker protein, dystonin, that is essential for maintaining neuronal cytoskeletal integrity. The db/db mouse has defective leptin receptors and the defects lead to impairments of leptin regulation of food intake and body weight, and result in the expression of diabetic symptoms such as hyperinsulinemia, hyperglicemia, and extreme obesity. In order to determine the effect of hereditary (in dt/dt mice) and metabolic disturbance (in db/db mice) on the morphology and nerve distribution of the vallate taste bud, a comparative study was performed among the wild type, dt/dt, and db/db mice, to examine the morphology at light and electron microscopic level, and distribution and abundance of the PGP-9.5 immunoreactivity in the taste buds of the vallate papilla. Morphometry and quantitative analysis on the distribution of taste buds and their gustatory nerve fibers are also demonstrated. Compared with wild type mice, the size of vallate papillae is much smaller in dt/dt mice (indicated by the total thickness of frontal sections, 330±19.25μm, vs. 240.3±20.07μm; n=3) and the number of taste buds decreased significantly (94.98±3.1, vs. 58.21±5.12 taste buds/papilla, n=3). However, in db/db mice, the morphology and size of vallate papilla (343±11.43μm, n=3) and the number of its taste buds (98.69±5.06 taste buds/papilla, n=3) are not apparently different from those of the wild type. The results from the PGP9.5 immunohistochemistry showed that the nerve innervation in taste bud cells was significantly reduced in dt/dt mice (25±4.02%, n=3), (indicated by proportion of PGP9.5 immunoreactive cells and fibers of the vallate papilla epithelium containing taste bud), as compared with wild type (47±2.84%, n=3) and db/db (48±8.79%, n=3) mice. Ultrastructural examination reveals four types of taste bud cells, i.e., type I, II, III and baseal cells. All of them express distinctive nuclear morphology, various cytoplasm electron density and characteristic subcellular organelles, in the vallate taste bud from the wild type and db/db mice. However, the cell density and nuclear morphology of the taste cells in dt/dt mice are not so distinct, and it is difficult to differentiate four types of taste bud cells at lower power electron microscopy, however, it is feasible at high power magnification. These findings confirmed our morphological findings at light microscopic level. We conclude that the sensory deficiency in the mutant dt/dt mice affects the morphology and innervations severely of taste buds, however, the metabolic disturbance of the mutant db/db mice does not interfere the structure and innervation of the taste buds in the vallate lingual papilla.