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Abstract

The effects of taurine in the mammalian nervous system are numerous and varied. There has been great difficulty in determining the specific targets of taurine action. The authors present a review of accepted taurine action and highlight recent discoveries regarding taurine and calcium homeostasis in neurons. In general there is a consensus that taurine is a powerful agent in regulating and reducing the intracellular calcium levels in neurons. After prolonged L-glutamate stimulation, neurons lose the ability to effectively regulate intracellular calcium. This condition can lead to acute swelling and lysis of the cell, or culminate in apoptosis. Under these conditions, significant amounts of taurine (mM range) are released from the excited neuron. This extracellular taurine acts to slow the influx of calcium into the cytosol through both transmembrane ion transporters and intracellular storage pools. Two specific targets of taurine action are discussed: Na(+)-Ca2+ exchangers, and metabotropic receptors mediating phospholipase-C.

Neuroprotective Mechanisms of Taurine against Ischemic Stroke

“…These observations were later supported by Frosini and colleagues [87]. There is also a strong possibility of there being two types of taurine receptor; an ionotropic taurine receptor [88] and a metabotropic taurine receptor [60]. Other researchers have also demonstrated the existence of distinct types of taurine receptor [226].…”

“…It has a multiple of neuroprotective mechanisms in the CNS such as: regulating cellular osmolarity [243,244], an anti-oxidant [65,66], neuromodulator of GABAergic transmission [85,245,246], maintaining calcium homeostasis [59,60,61,62,63], inhibiting glutamate excitotoxicity [59,69,133], attenuating endoplasmic reticulum stress [73,190,247], modulating the mitochondrial pore permeability [155] downregulating a range of pro-apoptotic proteins while upregulating anti-apoptotic proteins [70,176,179,248] and downregulating inflammatory mediators [217]. In ischemic stroke, a pathological brain condition, taurine is released in the extracellular space resulting in a decrease in the concentration of intracellular taurine.…”

“…The possibility of a metabotropic taurine receptor that is coupled to an inhibitory G-protein (Foos and Wu 2002 [60]) resulting in reduction of ER calcium release, maintaining the ER’s calcium homeostasis in the ischemic brain (Figure 3), could provide insights into taurine’s mechanism in reducing ER stress and ER stress-mediated apoptosis [73,190]. The neuroprotective mechanisms of taurine address the diverse pathological mechanisms observed in ischemic stroke.…”

“…In the CNS it plays a role in: neuromodulation [55,56,57], osmoregulation [33,58], the maintenance of calcium homeostasis [59,60,61,62,63], membrane stabilization [64], anti-oxidation [65,66], anti-inflammation [67,68] and neuroprotection [59,69,70,71,72,73] and is also seen as a trophic factor during CNS development [40,74]. Its neuroprotective effect is observed against l -glutamate induced excitotoxicity whereby it counteracts the glutamate-induced increase of intracellular calcium through L-, P/Q-, N-type voltage-gated calcium channels (VGCCs) and the N -methyl- d -aspartate (NMDA) receptor, thus preventing glutamate-induce membrane depolarization [59,69].…”

Site-specific sampling of taurine from rat brain followed by on-line sample pre-concentration, throughout in-capillary derivatization and capillary electrophoresis

“…To perform the site-specific sampling of a biological compound from a rat organ with the present method, we chose taurine and the rat brain as a standard, representative bioactive compound and organ for this study, because taurine is ubiquitous and is the most abundant, free, semi-essential amino acid in the mammalian heart [12], retina [13,14], skeletal muscle [15], brain [16,17] in leukocytes [18], etc. [19].…”