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J Physiol Volume 550, Number 3, 911-919, August 1, 2003 DOI: 10.1113/jphysiol.2003.045864
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J Physiol (2003), 550.3, pp. 911-919
© Copyright 2003 D 2003 The Physiological Society
DOI: 10.1113/jphysiol.2003.045864

Taurine-induced long-lasting enhancement of synaptic transmission in mice: role of transporters

O. A. Sergeeva*, A. N. Chepkova†, N. Doreulee*, K. S. Eriksson*, W. Poelchen*, I. Mönnighoff*, B. Heller-Stilb*, U. Warskulat‡, D. Häussinger‡ and H. L. Haas*

Departments of *Neurophysiology and ‡Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-Universität, PO Box 101007, D-40001 Düsseldorf, Germany, and †Brain Research Institute, Russian Academy of Medical Sciences, Moscow 103064, Russia

Taurine, a major osmolyte in the brain evokes a long-lasting enhancement (LLETAU) of synaptic transmission in hippocampal and cortico-striatal slices. Hippocampal LLETAU was abolished by the GABA uptake blocker nipecotic acid (NPA) but not by the taurine-uptake inhibitor guanidinoethyl sulphonate (GES). Striatal LLETAU was sensitive to GES but not to NPA. Semiquantitative PCR analysis and immunohistochemistry revealed that taurine transporter expression is significantly higher in the striatum than in the hippocampus. Taurine transporter-deficient mice displayed very low taurine levels in both structures and a low ability to develop LLETAU in the striatum, but not in the hippocampus. The different mechanisms of taurine-induced synaptic plasticity may reflect the different vulnerabilities of these brain regions under pathological conditions that are accompanied by osmotic changes such as hepatic encephalopathy.



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