CHOROID-PLEXUS TAURINE TRANSPORT

The putative osmoregulatory agent, taurine, is lost from the brain dur ing hypo-osmotic stress or ischemia, but the regulatory mechanisms inv olved in this loss have not been fully elucidated. In this study, we h ave examined taurine transport by the isolated rat choroid plexus, one element of the brain-blood interface, and examined how it may be regu lated as part of brain volume regulation. Choroid plexus taurine uptak e was Na- and Cl-dependent with a V-max and K-m of 6.5 +/- 0.3 pmol/mg /min and 232 +/- 33 mu M. The latter is substantially greater than the normal CSF taurine concentration and this may be important in removin g taurine released into the CSF during parenchymal cell swelling. Taur ine uptake also appears calmodulin dependent as it was reduced by 84 a nd 91% in the presence of 25 mu M trifluoperazine and 100 mu M W-7, tw o calmodulin inhibitors. Taurine efflux from choroid plexus was stimul ated by trifluoperazine, taurine, and hypo-osmotic stress. The latter two effects were reduced by niflumic acid, suggesting that taurine and hypo-osmotic stress act on the same pathway. The stimulation of efflu x by hypo-osmotic stress decreased with time, whereas the effect of ex ternal taurine was sustained. If this efflux pathway is involved in th e movement of taurine from choroid plexus to blood, these results sugg est that changes in extracellular taurine may be more important than t he direct effect of hypo-osmolality in the long-term loss of taurine f rom the brain.