Abstract
Directly after weaning, kittens were raised on a semisynthetic diet supplemented with 0.4% taurine or devoid of this amino acid. Eight to twelve weeks later the blood plasma concentration of taurine was decreased by 98-99% in kittens fed a taurine-free regimen. Parietal cortex dialysis, performed in anaesthetized kittens, revealed a selective, but less marked, reduction of extracellular taurine. When kainic acid was included in the dialysis buffer, taurine was doubled in taurine-supplemented kittens, but it was only slightly affected in deficient animals. The animals were also used for determination of the threshold of pentylenetetrazol-induced epilepsy 3 days after the dialysis experiment. This was not significantly different between the groups. The present work shows that taurine deficiency in its own right does not elevate interstitial glutamate, an effect previously observed in the 2-guanidino-ethane sulphonic acid model for taurine deficiency. The results further suggest that taurine is better retained in neural cells in the taurine-deficient state. Moreover, the findings argue against a role for endogenous taurine in the control of epileptiform discharge initiation and/or spread.