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This Article Full Text Full Text (PDF) All Versions of this Article: 585/2/539    most recent jphysiol.2007.141432v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Sergeeva, O. A. Articles by Haas, H. L. Search for Related Content PubMed PubMed Citation Articles by Sergeeva, O. A. Articles by Haas, H. L. Related Collections Neuroscience

Departments of
¹ Neurophysiology
² Gastroenterology, Hepatology & Infectiology
³ Neurology, Heinrich-Heine-University, POB 101007, D-40001 Düsseldorf, Germany

The Striatum is involved in the regulation of movements and motor skills. We have shown previously, that the osmolyte and neuromodulator taurine plays a role in striatal plasticity. We demonstrate now that hereditary taurine deficiency in taurine-transporter knock-out (TAUT KO) mice results in disinhibition of striatal network activity, which can be corrected by taurine supplementation. Modification of GABA_A but not glycine receptors (taurine is a ligand for both receptor types) underlies this disinhibition. Whole-cell recordings from acutely isolated as well as cultured striatal neurons revealed a decreased agonist sensitivity of the GABA_A receptor in TAUT KO neurons in the absence of changes in the maximal GABA-evoked current amplitude. The striatal GABA level in TAUT KO mice was unchanged. The amplitude enhancement of spontaneous IPSCs by zolpidem was stronger in TAUT KO than in wild-type (WT) animals. Tonic inhibition was absent in striatal neurons under control conditions but was detected after incubation with the GABA-transaminase inhibitor vigabatrin: bicuculline induced a larger shift of baseline current in WT as compared to TAUT KO neurons. Lack of taurine leads to reduced sensitivity of synaptic and extrasynaptic GABA_A receptors and consequently to disinhibition. These findings help in understanding neuropathologies accompanied by the loss of endogenous taurine, for instance in hepatic encephalopathy.

(Received 25 July 2007; accepted after revision 22 October 2007; first published online 25 October 2007)
Corresponding author O. Sergeeva: Heinrich-Heine-Universität, Physiology II, POB 101007, D-40001 Düsseldorf, Germany. Email: olga.sergeeva{at}uni-duesseldorf.de

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