Abstract
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 in vitro as well as neuronal migration in vitro and in vivo. 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.
Highlights
The aminosulfonic acid taurine (2-aminoethanesulfonic acid) is among the most abundant organic molecules in the human body, including the central nervous system (CNS), and has been attributed to a variety of physiological functions
Since taurine was not localized in the presynaptic structures and glycine was not released after electrical stimulation (Qian et al, 2014), these results suggest that, a substantial portion of this tangentially propagating activity transients is mediated by synaptic release of glycine and γ-aminobutyric acid (GABA), taurine acting on GABAA and glycine receptors in Cajal–Retzius cells (CRc) considerably contributed to the propagation of activity in the marginal zone (MZ) in a neuromodulatory fashion
Taurine can be considered as an important neurodevelopmental modulator (Figure 5)
Summary
The aminosulfonic acid taurine (2-aminoethanesulfonic acid) is among the most abundant organic molecules in the human body, including the CNS, and has been attributed to a variety of physiological functions (for review Huxtable, 1989; Lambert et al, 2015; Oja and Saransaari, 2015). A constitutive taurine release by electrical activity has been observed in the immature neocortex (Figure 1C; Qian et al, 2014) It is regularly stated, that taurine is a partial, low-affinity agonist on GABAA receptors (Albrecht and Schousboe, 2005). An interesting observation is that micromolar taurine concentrations can massively enhance tonic GABAergic currents, which suggest that extrasynaptic GABA and taurine may act synergistically (Ochoa-de la Paz et al, 2008) These observations indicate that specific subunit compositions of GABAA receptors can assemble high-affinity taurine receptors and indicate that even μM concentrations of taurine can be sufficient to mediate a physiologically relevant activation of ionotropic GABAA receptor subpopulations. On the other hand, loading experiments suggested that the taurine concentration could be as high as 1 mM in the embryonic neocortex (Furukawa et al, 2014)
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