大鼠轮廓乳头退化味蕾中的组织化学变化与细胞凋亡

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

作者信息

Ichimori Yasuo, Ueda Katsura, Okada Hiroyuki, Honma Shiho, Wakisaka Satoshi

机构信息

Department of Oral Anatomy and Developmental Biology, Osaka University Graduate School of Dentistry, Suita, Osaka, Japan.

出版信息

Arch Histol Cytol. 2009 Jul;72(2):91-100. doi: 10.1679/aohc.72.91.

Abstract

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 post-operative 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 beta2 subunit (PLCbeta2), 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 beta2-immunoreactive cells and cells showing no labeling for PLCbeta2, 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 PLCbeta2. 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.

摘要

本研究旨在检测双侧舌咽神经横断后大鼠轮廓乳头味蕾的组织化学变化及凋亡情况。舌咽神经横断后,味蕾数量在术后第3天(PO3)前未发生改变,但此后显著减少。然而,味蕾内细胞数量从PO2开始显著减少。在正常未损伤的动物中,分别约有15.4%、9.0%和7.7%的味蕾细胞被磷脂酶Cβ2亚基(PLCβ2,II型细胞标志物)、神经细胞黏附分子(NCAM,III型细胞标志物)和Jacalin(IV型细胞标志物)的抗体标记。味觉神经损伤后,表达III型和IV型细胞标志物的细胞比例从PO2开始逐渐降低,PO3时Jacalin标记的味蕾细胞消失。正常情况下,在PLCβ2免疫反应性细胞以及未被PLCβ2、NCAM或Jacalin标记的细胞的细胞核中可检测到单链DNA(ssDNA,凋亡标志物)的免疫反应性。在PO1时,显示ssDNA免疫反应性的味蕾细胞数量增加至正常未损伤动物的两倍;这些ssDNA免疫反应性细胞也被NCAM、Jacalin以及PLCβ2标记。目前的结果表明,味觉神经去神经支配会导致所有类型的味蕾细胞凋亡,从而导致味蕾迅速退化。

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