TY - JOUR
T1 - Na+- and Cl--Dependent transport of taurine at the blood-brain barrier
AU - Tamai, Ikumi
AU - Senmaru, Mizuho
AU - Terasaki, Tetsuya
AU - Tsuji, Akira
N1 - Funding Information:
Acknowledgements-The authorsth ankK imio Kirihara,M eat InspectionC entero f KanazawaC ity (KanazawaJ,a pan),f or providingf reshb ovineb rains.T his work was supportebdy a Grant-in-Aidf or ScientificR esearchfr om the Ministrvo f Education,S ciencea nd Culture,J apan,a grantf rom the Japan HealthS ciencesF oundationD, rugI nnovationP roject,a Grant-in-Aid for CancerR esearch(5 -14)f romt heM inistryo f Health andW elfare,a ndb y theT aishoP harmaceuticCaol . Ltd.
PY - 1995/11/27
Y1 - 1995/11/27
N2 - The characteristics of carrier-mediated transport of taurine at the blood-brain barrier (BBB) were studied by using primary cultured bovine brain capillary endothelial cells (BCECs), in situ brain perfusion and brain capillary depletion methods in rats. The uptake of [3H]taurine by cultured cells showed that the active transporter functions on both the luminal and antiluminal membranes of BCECs. The kinetic parameters for the saturable transport of taurine were estimated to be: for the luminal uptake, the Michaelis constant, Kv, was 12.1 ± 0.5 μM, and the maximum uptake rate, Jmax, was 4.32 ± 0.05 nmol/30 min/mg protein; for the antiluminal uptake, Kt was 13.6 ± 2.4 μM and Jmax was 2.81 ± 0.22 nmol/30 min/mg protein. The luminal and antiluminal uptakes of [3H]taurine were each dependent on both Na+ and Cl-. Stoichiometric analyses suggest that two Na+ and one Cl- are associated with the luminal uptake of one taurine molecule. β-Amino acids such as β-alanine and hypotaurine strongly inhibited the uptake of [3H]taurine, whereas α- and γ-amino acids had little or no effect. Furthermore, by in situ brain perfusion and in vivo brain capillary depletion methods, the carrier-mediated transport found by in vitro experiments was confirmed to function for the translocation of the taurine molecule from the vascular space into the brain. From these results, it was concluded that a Na+ and Cl- gradient-dependent transport (uptake) system for taurine exists in both the luminal and the antiluminal membranes of BCECs.
AB - The characteristics of carrier-mediated transport of taurine at the blood-brain barrier (BBB) were studied by using primary cultured bovine brain capillary endothelial cells (BCECs), in situ brain perfusion and brain capillary depletion methods in rats. The uptake of [3H]taurine by cultured cells showed that the active transporter functions on both the luminal and antiluminal membranes of BCECs. The kinetic parameters for the saturable transport of taurine were estimated to be: for the luminal uptake, the Michaelis constant, Kv, was 12.1 ± 0.5 μM, and the maximum uptake rate, Jmax, was 4.32 ± 0.05 nmol/30 min/mg protein; for the antiluminal uptake, Kt was 13.6 ± 2.4 μM and Jmax was 2.81 ± 0.22 nmol/30 min/mg protein. The luminal and antiluminal uptakes of [3H]taurine were each dependent on both Na+ and Cl-. Stoichiometric analyses suggest that two Na+ and one Cl- are associated with the luminal uptake of one taurine molecule. β-Amino acids such as β-alanine and hypotaurine strongly inhibited the uptake of [3H]taurine, whereas α- and γ-amino acids had little or no effect. Furthermore, by in situ brain perfusion and in vivo brain capillary depletion methods, the carrier-mediated transport found by in vitro experiments was confirmed to function for the translocation of the taurine molecule from the vascular space into the brain. From these results, it was concluded that a Na+ and Cl- gradient-dependent transport (uptake) system for taurine exists in both the luminal and the antiluminal membranes of BCECs.
KW - blood-brain barrier, cultured brain capillary endothelial cell
KW - carrier-mediated transport
KW - taurine
KW - β-amino acid
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U2 - 10.1016/0006-2952(95)02046-2
DO - 10.1016/0006-2952(95)02046-2
M3 - Article
C2 - 8615856
AN - SCOPUS:0029416927
VL - 50
SP - 1783
EP - 1793
JO - Biochemical Pharmacology
JF - Biochemical Pharmacology
SN - 0006-2952
IS - 11
ER -