Role of taurine in regulation of intracellular calcium level and neuroprotective function in cultured neurons

✍ Scribed by W.Q. Chen; H. Jin; M. Nguyen; J. Carr; Y.J. Lee; C.C. Hsu; M.D. Faiman; J.V. Schloss; J.Y. Wu

• Publisher: John Wiley and Sons
• Year: 2001
• Tongue: English
• Weight: 242 KB
• Volume: 66
• Category: Article
• ISSN: 0360-4012
• DOI: 10.1002/jnr.10027

✦ Synopsis

Abstract

Glutamate‐induced excitotoxicity has been implicated as an important mechanism underlying a variety of brain injuries and neurodegenerative diseases. Previously we have shown that taurine has protective effects against glutamate‐induced neuronal injury in cultured neurons. Here we propose that the primary underlying mechanism of the neuroprotective function of taurine is due to its action in preventing or reducing glutamate‐induced elevation of intracellular free calcium, [Ca^2+^]~i~. This hypothesis is supported by the following findings. First, taurine transport inhibitors, e.g., guanidinoethyl sulfonate and β‐alanine, have no effect on taurine's neuroprotective function, suggesting that taurine protects against glutamate‐induced neuronal damage through its action on the extracellular membranes. Second, glutamate‐induced elevation of [Ca^2+^]~i~ is reduced to the basal level upon addition of taurine. Third, pretreatment of cultured neurons with taurine prevents or greatly suppresses the elevation of [Ca^2+^]~i~ induced by glutamate. Furthermore, taurine was found to inhibit the influx but not the efflux of ^45^Ca^2+^ in cultured neurons. Taurine has little effect on the binding of [^3^H]glutamate to the agonist binding site and of [^3^H]MDL 105,519 to the glycine binding site of the N‐methyl‐D‐aspartic acid receptors, suggesting that taurine inhibits ^45^Ca^2+^ influx through other mechanisms, including its inhibitory effect on the reverse mode of the Na^+^/Ca^2+^ exchangers (Wu et al. [2000] In: Taurine 4: taurine and excitable tissues. New York: Kluwer Academic/Plenum Publishers. p 35–44) rather than serving as an antagonist to the N‐methyl‐D‐aspartic acid receptors. J. Neurosci. Res. 66:612–619, 2001. © 2001 Wiley‐Liss, Inc.