Ichikawa H, De Repentigny Y, Kothary R, Sugimoto T
Department of Oral Function and Anatomy, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama 700-8525, Japan.
Neuroscience. 2006;137(2):531-6. doi: 10.1016/j.neuroscience.2005.08.081. Epub 2005 Nov 14.
The vagal and glossopharyngeal sensory ganglia and their peripheral tissues were examined in wild type and dystonia musculorum mice to assess the effect of dystonin loss of function on chemoreceptive neurons. In the mutant mouse, the number of vagal and glossopharyngeal sensory neurons was severely decreased (70% reduction) when compared with wild type littermates. The mutation also reduced the size of the circumvallate papilla (45% reduction) and the number of taste buds (89% reduction). In addition, immunohistochemical analysis demonstrated that the dystonin mutation reduced the number of PGP 9.5-, calcitonin gene-related peptide-, P2X3 receptor- and tyrosine hydroxylase-containing neurons. Their peripheral endings also decreased in the taste bud and epithelium of circumvallate papillae. These data together suggest that the survival of vagal and glossopharyngeal sensory neurons is dependent upon dystonin.
在野生型和肌张力障碍小鼠中检查迷走神经和舌咽神经感觉神经节及其外周组织，以评估肌动蛋白功能丧失对化学感受神经元的影响。与野生型同窝小鼠相比，突变小鼠的迷走神经和舌咽神经感觉神经元数量严重减少（减少70%）。该突变还减小了轮廓乳头的大小（减少45%）和味蕾数量（减少89%）。此外，免疫组织化学分析表明，肌动蛋白突变减少了含PGP 9.5、降钙素基因相关肽、P2X3受体和酪氨酸羟化酶的神经元数量。它们的外周末梢在轮廓乳头的味蕾和上皮中也减少。这些数据共同表明，迷走神经和舌咽神经感觉神经元的存活依赖于肌动蛋白。
