US EPA

2453261 

Journal Article 

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

Lötsch, J; Hummel, T; Warskulat, U; Coste, O; Häussinger, D; Geisslinger, G; Tegeder, I 

2014 

1 

Neuroscience
ISSN: 0306-4522
EISSN: 1873-7544 

259 

63-70 

English 

24321512 

10.1016/j.neuroscience.2013.11.037 

WOS:000330597700008 

http://dx.doi.org/10.1016/j.neuroscience.2013.11.037
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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. 

pain; knock-out model; mice