Summary
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.
Résumé
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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References
Christensen O., 1987, Mediation of cell volume regulation by Cat+ influx through stretch-activated channels, Nature 330: 66–68.
Chung S. J., Ramanathan V., Giacomini K. M., and Brett C. M., 1994, Characterization of a sodium-dependent taurine transporter in rabbit choroid plexus., Biochim. Biophys. Acta 1193: 10–16.
Huxtable R. J., 1989, Taurine in the central nervous system and the mammalian actions of taurine., Prog. Neurobiol. 32: 471–533.
Keep R. F. and Xiang J., (in press), N-system amino acid transport at the blood-CSF barrier., J. Neurochem.
Keep R. F., Xiang J., and Betz A. L., 1994, Potassium cotransport at the rat choroid plexus., Am. J Physiol. 267: C1616 - C1622.
Lehmann A., Carlstrom C., Nagelhus E. A., and Ottersen O. P., 1991, Elevation of taurine in hippocampal extracellular fluid and cerebrospinal fluid of acutely hypoosmotic rats: contribution of influx from blood?, J. Neurochem. 56: 690–697.
Ohno K., Pettigrew K. D., and Rapoport S. 1., 1978, Lower limits of cerebrovascular permeability to nonelectrolytes in the conscious rat, Am J Physiol 235: H299 - H307.
Ramamoorthy S., Del Monte M. A., Leibach F. H., and Ganapathy V., 1994, Molecular identity and calmodulin-mediated regulation of the taurine transporter in a human retinal pigment epithelial cell line., Current Eye Res. 13: 523–529.
Schielke G. P., Moises H. C., and Betz A. L., 1990, Potassium activation of the Na,K-pump in isolated brain microvessels and synaptosomes, Brain Res 524: 291–296.
Semba J. and Patsalos P. N., 1993, Milacemide effects on the temporal inter-relationship of amino acids and monoamine metabolites in rat cerebrospinal fluid., Eur. J. Pharmacol. 230: 321–326.
Tayarani I., Cloez 1., Lefauconnier J.-M., and Bourre J.-M., 1989, Sodium-dependent high affinity uptake of taurine by isolated rat brain capillaries., Biochim. Biophys. Acta 985: 168–172.
Thurston J. H., Hauhart R. E., and Dirgo J. A., 1980, Taurine: a role in osmotic regulation of mammalian brain and possible clinical significance., Life Sci. 26: 1561–1568.
Verbalis J. G. and Gullans S. R., 1991, Hyponatremia causes large sustained reductions in brain content of multiple organic osmolytes in rats., Brain. Res. 567: 274–282.
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Keep, R.F., Stummer, W., Xiang, J., Betz, A.L. (1996). Blood-Brain Barrier Taurine Transport and Brain Volume Regulation. In: Couraud, PO., Scherman, D. (eds) Biology and Physiology of the Blood-Brain Barrier. Advances in Behavioral Biology, vol 46. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9489-2_3
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DOI: https://doi.org/10.1007/978-1-4757-9489-2_3
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