• J Lötsch, T Hummel, U Warskulat, O Coste, D Häussinger, G Geisslinger, and I Tegeder.
• Institute of Clinical Pharmacology, Goethe-University, Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany; Fraunhofer Institute of Molecular Biology and Applied Ecology-Project Group Translational Medicine and Pharmacology (IME-TMP), Theodor-Stern-Kai 7, D-60590 Frankfurt am Main, Germany. Electronic address: j.loetsch@em.uni-frankfurt.de.
• Neuroscience. 2014 Feb 14;259:63-70.

AbstractThe amino acid taurine is required for development and functioning of the central and peripheral nervous system where it exerts osmoregulatory, neuromodulatory and anti-apoptotic actions. It is subject to cellular import by the taurine transporter slc6a6. Absence of the transporter and consequently, absence of taurine leads to several neurologic deficits and sensory losses. In a slc6a6 knock-out mouse model, consequences of congenital taurine deficiency were assessed in nociceptive sensory processes. The formalin assay, hot plate assay, and summated generator potentials in response to local nociceptive stimulation with gaseous CO2 were applied. Reduced responsiveness of slc6a6(-/-) mice to nociceptive stimulation was observed in particular to chemical nociceptive stimuli. Scl6a6 knock-out mice spent significantly less time licking the formalin injected paw and displayed smaller amplitudes of the nociceptive nasal mucosa potentials than wild-type mice (p=0.002 and 0.01 respectively). In contrast, withdrawal latencies on a hot plate did not significantly differ, suggesting that intracellular taurine deficits lead in particular to a hyposensitivity of nociceptive sensory neurons sensitive to noxious chemical stimulation. As hereditary absence of taurine affects biological processes of anatomical structure development, the altered nociceptive responses likely reflect consequences of compromised peripheral nervous system development.Copyright © 2013 IBRO. Published by Elsevier Ltd. All rights reserved.

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