Blood-Brain Barrier Taurine Transport and Brain Volume Regulation

  • Richard F. Keep
  • Walter Stummer
  • Jianming Xiang
  • A. Lorris Betz
Part of the Advances in Behavioral Biology book series (ABBI, volume 46)


We have investigated mechanisms that may be involved in brain taurine loss during hypo-osmotic stress using a mixture of in vivo and in vitro measurements of blood-brain and blood-CSF barrier taurine transport. Choroid plexus taurine uptake has a Km of 230 µM, indicating that it is not saturated at normal CSF concentrations and that uptake will increase as extracellular taurine concentration increases. Choroid plexus uptake was reduced in the presence of calmodulin inhibitors suggesting that calmodulin may be involved in brain volume regulation. Choroid plexus 3H-taurine efflux via a niflumic acid-sensitive pathway was stimulated directly by reductions in osmolality and also by increases in extracellular taurine. Unlike other tissues, efflux was not stimulated by hypo-osmotic stress in isolated cerebral microvessels. This may indicate that such an efflux mechanism is, if present at all, on the luminal membrane and not accessible in these experiments. Although plasma taurine was increased by hypo-osmotic stress in vivo, this was not reflected by an increase in taurine influx across the blood-brain barrier. Thus this barrier tissue also prevents taurine from being recycled back into brain.


Osmotic Stress Choroid Plexus Taurine Concentration Cerebral Microvessels Taurine Uptake 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Nous avons étudié les mécanismes qui pourraient expliquer la déperdition du cerveau en taurine au cours de chocs hypo-osmotiques par des expériences de mesure du transport de la taurine par la barrière entre le sang et le parenchyme cérébral (BHE) et la barrière entre le sang et le liquide céphalo-rachidien (plexus choroïdes). La captation de la taurine par les plexus choroïdes possède un Km de 230 µM, indiquant que le transport de taurine n’est pas saturé aux concentrations normales présentes dans le liquide cephalo-rachidien. De ce fait, une augmentation extracellulaire de la concentration en taurine s’accompagnera d’une élévation du transport de taurine au niveau des plexus choroïdes. Des inhibiteurs de la calmoduline provoquent une réduction du transport par les plexus choroïdes suggérant que la calmoduline pourrait être impliquée dans la régulation du volume cérébral. L’efflux de taurine tritiée par les plexus choroïdes, via une voie sensible à l’acide niflumique, est stimulée directement par une diminution de l’osmolarité mais aussi par une augmentation de la concentration de la taurine extracellulaire. Dans des microvaisseaux cérébraux isolés, cet efflux n’est pas stimulé par un choc hypo-osmotique.

Ces résultats pourraient indiquer que l’efflux de la taurine, s’il existe au niveau des microvaisseaux cérébraux ne se produit qu’au niveau de leur membrane luminale non accessible dans des expériences utilisant des capillaires cérébraux isolés. Bien que la concentration plasmatique de taurine augmente in vivo lors des chocs hypo-osmotiques, cela ne se traduit pas par une augmentation du transport de la taurine par la BHE. Ainsi, la BHE empêche aussi la taurine d’être recyclée vers le cerveau.


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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  • Richard F. Keep
    • 1
  • Walter Stummer
    • 1
  • Jianming Xiang
    • 1
  • A. Lorris Betz
    • 1
    • 2
  1. 1.Department of Surgery (Neurosurgery)University of MichiganAnn ArborUSA
  2. 2.Departments of Pediatrics and NeurologyUniversity of MichiganAnn ArborUSA

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