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Taste bud-derived BDNF maintains innervation of a subset of TrkB-expressing gustatory nerve fibers.
Molecular and Cellular Neuroscience ( IF 3.5 ) Pub Date : 2017-06-11 , DOI: 10.1016/j.mcn.2017.06.001
Tao Tang 1 , Jennifer Rios-Pilier 1 , Robin Krimm 1
Affiliation  

Taste receptor cells transduce different types of taste stimuli and transmit this information to gustatory neurons that carry it to the brain. Taste receptor cells turn over continuously in adulthood, requiring constant new innervation from nerve fibers. Therefore, the maintenance of innervation to taste buds is an active process mediated by many factors, including brain-derived neurotrophic factor (BDNF). Specifically, 40% of taste bud innervation is lost when Bdnf is removed during adulthood. Here we speculated that not all gustatory nerve fibers express the BDNF receptor, TrkB, resulting in subsets of neurons that vary in their response to BDNF. However, it is also possible that the partial loss of innervation occurred because the Bdnf gene was not effectively removed. To test these possibilities, we first determined that not all gustatory nerve fibers express the TrkB receptor in adult mice. We then verified the efficiency of Bdnf removal specifically in taste buds of K14-CreER:Bdnf mice and found that Bdnf expression was reduced to 1%, indicating efficient Bdnf gene recombination. BDNF removal resulted in a 55% loss of TrkB-expressing nerve fibers, which was greater than the loss of P2X3-positive fibers (39%), likely because taste buds were innervated by P2X3+/TrkB- fibers that were unaffected by BDNF removal. We conclude that gustatory innervation consists of both TrkB-positive and TrkB-negative taste fibers and that BDNF is specifically important for maintaining TrkB-positive innervation to taste buds. In addition, although taste bud size was not affected by inducible Bdnf removal, the expression of the γ subunit of the ENaC channel was reduced. So, BDNF may regulate expression of some molecular components of taste transduction pathways.

中文翻译:

味蕾来源的BDNF维持表达TrkB的味觉神经纤维的一部分的神经支配。

味觉受体细胞转导不同类型的味觉刺激,并将该信息传递到味觉神经元,然后将其传递到大脑。味觉受体细胞在成年期不断翻身,需要神经纤维不断提供新的神经支配。因此,维持味蕾的神经支配是由许多因素介导的活跃过程,包括脑源性神经营养因子(BDNF)。具体而言,在成年期去除Bdnf会损失40%的味蕾神经。在这里我们推测并不是所有的味觉神经纤维都表达BDNF受体TrkB,从而导致神经元对BDNF的反应有所不同。但是,也有可能由于未有效去除Bdnf基因而导致部分神经支配丧失。为了测试这些可能性,我们首先确定并不是所有的味觉神经纤维都在成年小鼠中表达TrkB受体。然后,我们验证了K14-CreER:Bdnf小鼠味蕾中Bdnf去除的效率,发现Bdnf表达降低到1%,表明Bdnf基因重组有效。BDNF的去除导致表达TrkB的神经纤维损失55%,大于P2X3阳性纤维的损失(39%),这可能是因为味蕾由不受BDNF去除影响的P2X3 + / TrkB-纤维所支配。我们得出结论,味觉神经支配由TrkB阳性和TrkB负味纤维组成,而BDNF对于维持TrkB阳性对味蕾的神经特别重要。此外,尽管味蕾的大小不受诱导性Bdnf去除的影响,减少了ENaC通道的γ亚基的表达。因此,BDNF可能调节味觉传导途径的某些分子成分的表达。
更新日期:2019-11-01
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