Congenital taurine deficiency in mice is associated with reduced sensitivity to nociceptive chemical stimulation

• Published in: Neuroscience Vol. 259; pp. 63 - 70
• Main Authors: Lötsch, J., Hummel, T., Warskulat, U., Coste, O., Häussinger, D., Geisslinger, G., Tegeder, I.
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier Ltd 14.02.2014; Elsevier
• Subjects: Analysis of Variance; Animals; Biological and medical sciences; Carbon Dioxide - pharmacology; Formaldehyde - adverse effects; Fundamental and applied biological sciences. Psychology; Hyperalgesia - genetics; Hyperalgesia - physiopathology; knock-out model; Membrane Glycoproteins - deficiency; Membrane Transport Proteins - deficiency; Mice; Mice, Inbred C57BL; Mice, Knockout; Neurology; Nociception - physiology; pain; Pain Measurement - drug effects; Pain Threshold - physiology; Somesthesis and somesthetic pathways (proprioception, exteroception, nociception); interoception; electrolocation. Sensory receptors; Stimulation, Chemical; Taurine - metabolism; Time Factors; Vertebrates: nervous system and sense organs; NMP; HSAN; pain; rm-ANOVA; knock-out model; mice; analysis of variance for repeated measures; negative mucosa potential; hereditary sensory and autonomic neuropathy; Nociception; Taurine; Rodentia; Stimulation; Vertebrata; Sensitivity; Mammalia; Pain; Mouse; Animal; Models
• ISSN: 0306-4522; 1873-7544; 1873-7544
• DOI: 10.1016/j.neuroscience.2013.11.037

•Chronic loss of intracellular taurine leads to neuro-sensory deficits.•This extends to the responses to chemical nociceptive stimuli.•Taurine transport might be a novel target of analgesics. The 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.