Department of Psychology, University of Virginia, Charlottesville, Virginia 22904-4400 and.
Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky 40292.
J Neurosci. 2018 Aug 1;38(31):6873-6887. doi: 10.1523/JNEUROSCI.0802-18.2018. Epub 2018 Jun 28.
The rodent peripheral gustatory system is especially plastic during early postnatal development and maintains significant anatomical plasticity into adulthood. Thus, taste information carried from the tongue to the brain is built and maintained on a background of anatomical circuits that have the capacity to change throughout the animal's lifespan. Recently, the neurotrophin brain-derived neurotrophic factor (BDNF) was shown to be required in the tongue to maintain normal levels of innervation in taste buds at adulthood, indicating that BDNF is a key molecule in the maintenance of nerve/target matching in taste buds. Here, we tested whether maintenance of the central process of these gustatory nerves at adulthood also relies on BDNF by using male and female transgenic mice with inducible CreERT2 under the control of the keratin 14 promoter or under control of the ubiquitin promoter to remove from the tongue or from all tissues, respectively. We found that the terminal fields of gustatory nerves in the nucleus of the solitary tract were expanded when was removed from the tongue at adulthood and with even larger and more widespread changes in mice where was removed from all tissues. Removal of did not affect numbers of ganglion cells that made up the nerves and did not affect peripheral, whole-nerve taste responses. We conclude that normal expression of in gustatory structures is required to maintain normal levels of innervation at adulthood and that the central effects of removal are opposite of those in the tongue. BDNF plays a major role in the development and maintenance of proper innervation of taste buds. However, the importance of BDNF in maintaining innervation patterns of gustatory nerves into central targets has not been assessed. Here, we tested whether removal from the tongue or from all structures in adult mice impacts the maintenance of how taste nerves project to the first central relay. Deletion of from the tongue and from all tissues led to a progressively greater expansion of terminal fields. This demonstrates, for the first time, that BDNF is necessary for the normal maintenance of central gustatory circuits at adulthood and further highlights a level of plasticity not seen in other sensory system subcortical circuits.
啮齿动物的外周味觉系统在出生后早期发育阶段特别具有可塑性,并在成年期保持显著的解剖可塑性。因此,从舌头传递到大脑的味觉信息是在具有改变整个动物生命周期的解剖回路的背景上构建和维持的。最近,神经营养因子脑源性神经营养因子(BDNF)被证明在舌头上是维持成年期味觉感受器正常神经支配所必需的,这表明 BDNF 是维持味觉感受器中神经/靶匹配的关键分子。在这里,我们通过使用分别由角蛋白 14 启动子或泛素启动子控制的诱导型 CreERT2 的雄性和雌性转基因小鼠来测试这些味觉神经的中央过程在成年期是否也依赖于 BDNF,以分别从舌头上或从所有组织中去除 。我们发现,当成年期从舌头上去除 时,味觉神经的终末场在孤束核中扩大,而在从所有组织中去除 时,终末场的变化更大且更广泛。去除 并不影响构成神经的神经节细胞的数量,也不影响周围的、全神经味觉反应。我们得出结论,正常表达的 味觉结构是维持成年期正常神经支配所必需的,而 去除的中枢效应与舌头上的相反。BDNF 在味觉感受器的发育和维持正常神经支配中起着重要作用。然而,BDNF 在维持味觉神经向中枢靶标传入的神经支配模式中的重要性尚未得到评估。在这里,我们测试了成年小鼠从舌头上或从所有结构中去除 是否会影响味觉神经向第一中枢中继投射的维持。从舌头上和所有组织中删除 导致终末场逐渐扩大。这首次表明,BDNF 是成年期正常维持中枢味觉回路所必需的,进一步强调了在其他感觉系统皮质下回路中未见的可塑性水平。