Taurine in the anterior cingulate cortex diminishes neuropathic nociception: A possible interaction with the glycine A receptor

• Published in: European journal of pain 2007-05, Vol.11 (4), p.444-451
• Main Authors: Pellicer, Francisco, López-Avila, Alberto, Coffeen, Ulises, Manuel Ortega-Legaspi, J., Ángel, Rosendo del
• Format: Article
• Language: English
• Subjects: Animals; Anterior cingulate cortex; Autotomy; Behavior, Animal - physiology; Glycine Agents - administration & dosage; Glycine Agents - pharmacology; Glycine receptor; Gyrus Cinguli - physiology; Male; Microinjections; Pain; Pain - drug therapy; Pain - etiology; Pain - psychology; Pain Measurement - drug effects; Peripheral Nervous System Diseases - complications; Rats; Rats, Wistar; Receptors, Glycine - antagonists & inhibitors; Receptors, Glycine - drug effects; Strychnine; Strychnine - administration & dosage; Strychnine - pharmacology; Taurine; Taurine - administration & dosage; Taurine - therapeutic use
• ISSN: 1090-3801; 1532-2149
• DOI: 10.1016/j.ejpain.2006.06.003

Taurine is an inhibitory amino-acid which has been proposed as a nociceptive process neuromodulator. The glycine A receptor (glyR A) has been postulated as a receptor in which taurine exerts its function. Functional image studies have documented the role of the anterior cingulate cortex (ACC) in the affective component of pain. The aim of this study was to investigate the role of taurine as a glycinergic agonist in the ACC using a neuropathic pain model related to autotomy behaviour (AB). In order to test whether glyR A is responsible for taurine actions, we microinjected strychnine, a glyR A antagonist. We used taurine microinjected into the ACC, followed by a thermonociceptive stimulus and a sciatic denervation. Chronic nociception was measured by the autotomy score, onset and incidence. The administration of taurine 7 days after denervation modifies the temporal course of AB by inhibiting it. Our results showed a decreased autotomy score and incidence in the taurine groups, as well as a delay in the onset. Those experimental groups in which strychnine was microinjected into the ACC, either on its own or before the microinjection of taurine, showed no difference as compared to the control group. When taurine was microinjected prior to strychnine, the group behaved as if only taurine had been administered. Our results evidence a significant neuropathic nociception relief measured as an AB decrease by the microinjection of taurine into the ACC. Besides, the role of the glyR A is evidenced by the fact that strychnine antagonises the antinociceptive effect of taurine.