小鼠腭形味觉上皮和味蕾的形态发生需要依赖bdnf的味觉神经元

Oakley, Brandemihl, Cooper, Lau, Lawton, Zhang
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引用次数: 0

摘要

脑源性神经营养因子(BDNF)在零突变小鼠的发育缺失导致了三种相关的味觉乳头缺陷:神经支配稀疏、味觉上皮面积减少和味蕾减少。出生后第7天,bdnf零突变小鼠发育不良的乳突比野生型小鼠窄30%,沟壁面积缩小35%,味蕾数量减少75%。我们对神经支配密度进行了定量评估,以确定小沟壁和味蕾缺失是否可能是味觉神经元耗损的继发性后果。味觉神经支配减少与沟壁面积减少(r=+0.94)和味蕾减少(r=+0.96)呈线性相关。残余的味蕾比正常的小,由少数存活的味觉神经元支配。我们得出结论,bdnf依赖性味觉神经元有助于舌味觉上皮的形态发生,并且是产前和产后哺乳动物味蕾形成所必需的。味觉系统提供了一个明显的感觉器官形态发生受损的例子,这是继发于由神经营养因子基因零突变引起的感觉神经元耗竭。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The morphogenesis of mouse vallate gustatory epithelium and taste buds requires BDNF-dependent taste neurons

The developmental absence of brain-derived neurotrophic factor (BDNF) in null mutant mice caused three interrelated defects in the vallate gustatory papilla: sparse innervation, a reduction in the area of the gustatory epithelium, and fewer taste buds. On postnatal day 7, the stunted vallate papilla of bdnf null mutant mice was 30% narrower, the trench walls 35% reduced in area, and the taste buds 75% less abundant compared with wild-type controls. Quantitative assessment of innervation density was carried out to determine if the small trench walls and shortage of taste buds could be secondary consequences of the depletion of gustatory neurons. The diminished gustatory innervation was linearly associated with a reduced trench wall area (r=+0.94) and fewer taste buds (r=+0.96). Residual taste buds were smaller than normal and were innervated by a few surviving taste neurons. We conclude that BDNF-dependent taste neurons contribute to the morphogenesis of lingual gustatory epithelia and are necessary for both prenatal and postnatal mammalian taste bud formation. The gustatory system provides a conspicuous example of impaired sense organ morphogenesis that is secondary to sensory neuron depletion by neurotrophin gene null mutation.

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