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Received April 27, 2003
Accepted after revision May 12, 2003
1 Heinrich-Heine-Universität, Physiology II, PO Box 101007, D-40001 Düsseldorf, Germany
2 Brain Research Institute, Russian Academy of Medical Sciences, Moscow 103064, Russia
3 Department of Neurophysiology, Hepatology and Infectiology, Heinrich-Heine-Universität, PO Box 101007, D-40001 Düsseldorf, Germany
4 Department of Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-Universität, PO Box 101007, D-40001 Düsseldorf, Germany
5 Department of Neurophysiology , Hepatology and Infectiology, Heinrich-Heine-Universität, PO Box 101007, D-40001 Düsseldorf, Germany
* To whom correspondence should be addressed. E-mail: olga.sergeeva{at}uni-duesseldorf.de.
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. Thus the different mechanisms of taurine uptake in the striatum and hippocampus may be relevant to taurine-induced synaptic plasticity and the different vulnerabilities of these brain regions under pathological conditions that are accompanied by osmotic changes such as hepatic encephalopathy.
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