Abstract

Developmental patterns and pharmacological and biochemical properties of taurine transport system were investigated using developing primary cultured neurons prepared from mouse cerebral cortex by trypsin treatment. [ 3H]Taurine was incorporated into neurons via a high-affinity transport system of which the K m value as well as the V max value increased during neuronal development in vitro. This transport system was also inhibited by sodium withdrawal from incubation medium and exposures for 15 h to several metabolic inhibitors such as 2,4-dinitrophenol and monoiodoacetate. In addition, [ 3H]taurine uptake in both neurons cultured for 3 and 14 days was competitively inhibited by β-alanine, guanidinoethanesulfonate and hypotaurine. Cysteic acid and cysteine sulfinic acid, metabolic intermediates produced in the process of taurine biosynthesis in the brain from cysteine, induced significant reductions in [ 3H]taurine uptake in both types of cultured neurons, while cysteine, isethionic acid, cysteamine and cystamine exhibited no alterations in [ 3H]taurine transport. Moreover, non-competitive inhibition of [ 3H]taurine uptake by cysteic acid was observed in both neurons. These results clearly indicate that taurine uptake was mediated by the sodium- and energy-dependent transport system with high affinity in 14-day-old neurons as well as neurons cultured for 3 days and that both the K m and V max values of this transport system increase during neuronal development in vitro. The results described above suggest that the decrease in taurine content observed in developing brain is unlikely to be due to alteration in the capacity of the taurine transport system during neuronal development.

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