Montaño J A, Calavia M G, García-Suárez O, Suarez-Quintanilla J A, Gálvez A, Pérez-Piñera P, Cobo J, Vega J A
Departamento de Ciencias de la Salud, Universidad Católica San Antonio, Murcia, Spain.
Neurosci Lett. 2009 Oct 2;463(2):114-8. doi: 10.1016/j.neulet.2009.07.073. Epub 2009 Jul 29.
Pacinian corpuscles are innervated by large myelinated Aalpha-beta axons from the large- and intermediate-sized sensory neurons of dorsal root ganglia. These neurons express different members of the degenerin/epithelial Na(+) channel (DEG/ENa(+)C) superfamily of proteins with putative mechanosensory properties, whose expression is regulated by the TrkB-BDNF system. Thus, we hypothesized that BDNF and/or NT-4 signalling through activation of TrkB may regulate the expression of molecules supposed to be necessary for the mechanosensory function of Pacinian corpuscles. To test this hypothesis we analyzed the expression and distribution of ENa(+)C subunits and acid-sensing ion channel 2 (ASIC2) in Pacinian corpuscles from 25 days old mice deficient in TrkB, BDNF and NT-4. Pacinian corpuscles in these animals are normal in number, structure, and expression of several immunohistochemical markers. Using immunohistochemistry we observed that the beta-ENa(+)C and gamma-ENa(+)C subunits, but not the alpha-ENa(+)C subunit, were expressed in wild-type animals, and they were always found in the central axon. ASIC2 immunoreactivity was found in both the central axon and the inner core cells. The absence of TrkB or BDNF abolished expression of beta-ENa(+)C and ASIC2, whereas expression of gamma-ENa(+)C did not change. Expression of beta-ENa(+)C and gamma-ENa(+)C subunits in NT-4 deficient mice was found in the axons but also in the inner core cells whereas levels of expression of ASIC2 were increased in these animals. This study suggests that expression in Pacianian corpuscles of some potential mechanosensory proteins is regulated by BDNF, NT-4 and TrkB.
环层小体由背根神经节中大、中型感觉神经元发出的有髓鞘的大Aα-β轴突支配。这些神经元表达具有假定机械感觉特性的退化蛋白/上皮钠通道（DEG/ENaC）超家族的不同成员，其表达受TrkB-BDNF系统调节。因此，我们推测通过激活TrkB的BDNF和/或NT-4信号可能调节环层小体机械感觉功能所需分子的表达。为了验证这一假设，我们分析了25日龄缺乏TrkB、BDNF和NT-4的小鼠环层小体中ENaC亚基和酸敏感离子通道2（ASIC2）的表达和分布。这些动物的环层小体在数量、结构和几种免疫组织化学标记物的表达上均正常。通过免疫组织化学我们观察到，β-ENaC和γ-ENaC亚基而非α-ENaC亚基在野生型动物中表达，且它们总是存在于中央轴突中。ASIC2免疫反应性在中央轴突和内核细胞中均有发现。TrkB或BDNF的缺失消除了β-ENaC和ASIC2的表达，而γ-ENaC的表达没有变化。在NT-4缺陷小鼠中，β-ENaC和γ-ENaC亚基在轴突中以及内核细胞中均有表达，而这些动物中ASIC2的表达水平增加。这项研究表明，环层小体中一些潜在的机械感觉蛋白的表达受BDNF、NT-4和TrkB调节。
