Choroid plexus histidine transport

System-N transport plays an important role in L-glutamine uptake into isolated rat choroid plexus but its role in the transport of another System-N substrate, L-histidine, has yet to be determined. Similarly, the possible effects on System-N mediated L-histidine transport of changes in pH and extracellular L-glutamine, such as occur in cerebral ischemia and hepatic encephalopathy, have yet to be examined. In the absence of competing amino acids, L-[H-3]histidine uptake in isolated rat choroid plexus was mediated by both Na+-independent and Na+-dependent transport. The former was inhibited by 2-amino-2-norbornane carboxlic acid, indicating System-L transport, while the latter appears System-N mediated as it was inhibited by three System-N substrates but not substrates for System-A and -ASC. The Na+-dependent uptake had a K-m of 0.2 mM and a V-max of 1.4 nmol/mg/min. It accounted for 30% of L-histidine uptake in the presence of physiological concentrations of amino acids. Reductions in pH markedly inhibited Na+-dependent but not Na+-independent transport indicating that, as in liver but not neurons, System-N mediated transport at the choroid plexus is pH sensitive. Increases in L-glutamine concentration in the pathophysiological range reduced L-histidine uptake via both System-L and -N. (C) 1998 Elsevier Science B.V.