Kilb Werner, Fukuda Atsuo
Institute of Physiology, University Medical Center, Johannes Gutenberg University of Mainz, Mainz, Germany.
Department of Neurophysiology, Hamamatsu University School of Medicine, Hamamatsu, Japan.
Front Cell Neurosci. 2017 Oct 24;11:328. doi: 10.3389/fncel.2017.00328. eCollection 2017.
A variety of experimental studies demonstrated that neurotransmitters are an important factor for the development of the central nervous system, affecting neurodevelopmental events like neurogenesis, neuronal migration, programmed cell death, and differentiation. While the role of the classical neurotransmitters glutamate and gamma-aminobutyric acid (GABA) on neuronal development is well established, the aminosulfonic acid taurine has also been considered as possible neuromodulator during early neuronal development. The purpose of the present review article is to summarize the properties of taurine as neuromodulator in detail, focusing on the direct involvement of taurine on various neurodevelopmental events and the regulation of neuronal activity during early developmental epochs. The current knowledge is that taurine lacks a synaptic release mechanism but is released by volume-sensitive organic anion channels and/or a reversal of the taurine transporter. Extracellular taurine affects neurons and neuronal progenitor cells mainly via glycine, GABA(A), and GABA(B) receptors with considerable receptor and subtype-specific affinities. Taurine has been shown to directly influence neurogenesis as well as neuronal migration . It provides a depolarizing signal for a variety of neuronal population in the immature central nervous system, thereby directly influencing neuronal activity. While in the neocortex, taurine probably enhance neuronal activity, in the immature hippocampus, a tonic taurinergic tone might be necessary to attenuate activity. In summary, taurine must be considered as an essential modulator of neurodevelopmental events, and possible adverse consequences on fetal and/or early postnatal development should be evaluated for pharmacological therapies affecting taurinergic functions.
各种实验研究表明，神经递质是中枢神经系统发育的一个重要因素，影响神经发生、神经元迁移、程序性细胞死亡和分化等神经发育事件。虽然经典神经递质谷氨酸和γ-氨基丁酸（GABA）在神经元发育中的作用已得到充分证实，但氨基磺酸牛磺酸在神经元早期发育过程中也被认为是一种可能的神经调节剂。本综述文章的目的是详细总结牛磺酸作为神经调节剂的特性，重点关注牛磺酸在各种神经发育事件中的直接作用以及早期发育阶段神经元活动的调节。目前的认识是，牛磺酸缺乏突触释放机制，但可通过容积敏感性有机阴离子通道和/或牛磺酸转运体的反向转运而释放。细胞外牛磺酸主要通过甘氨酸、GABA（A）和GABA（B）受体影响神经元和神经祖细胞，具有相当的受体和亚型特异性亲和力。牛磺酸已被证明可直接影响神经发生以及神经元迁移。它为未成熟中枢神经系统中的多种神经元群体提供去极化信号，从而直接影响神经元活动。在新皮层中，牛磺酸可能增强神经元活动，而在未成熟的海马体中，可能需要持续的牛磺酸能张力来减弱活动。总之，必须将牛磺酸视为神经发育事件的重要调节剂，对于影响牛磺酸能功能的药物治疗，应评估其对胎儿和/或出生后早期发育可能产生的不良后果。
