Departamento de Farmacobiología, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional, Ciudad de México, México.
Laboratorio de Neurobiología Molecular y Celular de la Glía, Unidad de Investigación UNAM-APEC, México City, México.
PLoS One. 2024 Jun 24;19(6):e0305853. doi: 10.1371/journal.pone.0305853. eCollection 2024.
The intricate process of neuronal differentiation integrates multiple signals to induce transcriptional, morphological, and electrophysiological changes that reshape the properties of neural precursor cells during their maturation and migration process. An increasing number of neurotransmitters and biomolecules have been identified as molecular signals that trigger and guide this process. In this sense, taurine, a sulfur-containing, non-essential amino acid widely expressed in the mammal brain, modulates the neuronal differentiation process. In this study, we describe the effect of taurine acting via the ionotropic GABAA receptor and the metabotropic GABAB receptor on the neuronal differentiation and electrophysiological properties of precursor cells derived from the subventricular zone of the mouse brain. Taurine stimulates the number of neurites and favors the dendritic complexity of the neural precursor cells, accompanied by changes in the somatic input resistance and the strength of inward and outward membranal currents. At the pharmacological level, the blockade of GABAA receptors inhibits these effects, whereas the stimulation of GABAB receptors has no positive effects on the taurine-mediated differentiation process. Strikingly, the blockade of the GABAB receptor with CGP533737 stimulates neurite outgrowth, dendritic complexity, and membranal current kinetics of neural precursor cells. The effects of taurine on the differentiation process involve Ca2+ mobilization and the activation of intracellular signaling cascades since chelation of intracellular calcium with BAPTA-AM, and inhibition of the CaMKII, ERK1/2, and Src kinase inhibits the neurite outgrowth of neural precursor cells of the subventricular zone.
神经元分化的复杂过程整合了多种信号,诱导转录、形态和电生理变化,重塑神经前体细胞在成熟和迁移过程中的特性。越来越多的神经递质和生物分子被确定为触发和指导这一过程的分子信号。在这个意义上,牛磺酸是一种广泛存在于哺乳动物大脑中的含硫非必需氨基酸,它调节神经元分化过程。在这项研究中,我们描述了牛磺酸通过离子型 GABA A 受体和代谢型 GABA B 受体发挥作用对源自小鼠脑室下区的前体细胞的神经元分化和电生理特性的影响。牛磺酸刺激神经突的数量,并有利于神经前体细胞的树突复杂性,同时改变体细胞输入电阻和内向和外向膜电流的强度。在药理学水平上,GABAA 受体的阻断抑制了这些效应,而 GABA B 受体的刺激对牛磺酸介导的分化过程没有积极影响。引人注目的是,用 CGP533737 阻断 GABA B 受体刺激神经前体细胞的神经突生长、树突复杂性和膜电流动力学。牛磺酸对分化过程的影响涉及钙动员和细胞内信号级联的激活,因为 BAPTA-AM 螯合细胞内钙以及钙调蛋白激酶 II(CaMKII)、细胞外信号调节激酶 1/2(ERK1/2)和Src 激酶的抑制抑制了室下区神经前体细胞的神经突生长。