Abstract
Taurine (Tau) i the CNS has been suggested to serve as an osmoregulator, inhibitory neuromodulator or neurotransmitter 1. Suppositions regarding the functions of Tau have been associated with its readiness to become released from astrocytes or neurons in response to a plethora of pathological and physiological stimuli 1, also including pathologic concentrations of ammonia 3,4. Two distinct mechanisms have been shown to underlie Tau transport across the plasma membrane: a) opening or activation of volume-operated anion channels (VSOAC), which subserves Tau efflux, b) activation of a specific taurine carrier - TauT, often associated with increased expression of TauT mTNA5,6.
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Zielinska, M., Zablocka, B., Albrecht, J. (2003). Effect of Ammonia on Taurine Transport in C6 Glioma Cells. In: Lombardini, J.B., Schaffer, S.W., Azuma, J. (eds) Taurine 5. Advances in Experimental Medicine and Biology, vol 526. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0077-3_55
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DOI: https://doi.org/10.1007/978-1-4615-0077-3_55
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