• Giuliano Taccola, Pierre J Doyen, Jonathan Damblon, Nejada Dingu, Beatrice Ballarin, Arnaud Steyaert, Rieux Anne des AD Louvain Drug Research Institute, Av. Mounier 73, Brussels and Institute of Condensed Matter and Nanosciences, Université catholique de Louvain, 1348 Lou, Patrice Forget, Emmanuel Hermans, Barbara Bosier, and Ronald Deumens.
• Institute of Neuroscience, Université catholique de Louvain, Av. Hippocrate 54, Brussels, Belgium; Neuroscience Department, International School for Advanced Studies (SISSA), via Bonomea 265, Trieste, TS, Italy; SPINAL (Spinal Person Injury Neurorehabilitation Applied Laboratory), Istituto di Medicina Fisica e Riabilitazione (IMFR), via Gervasutta 48, Udine (UD), Italy.
• Exp. Neurol. 2016 Dec 1; 286: 1-11.

AbstractTactile hypersensitivity is one of the most debilitating symptoms of neuropathic pain syndromes. Clinical studies have suggested that its presence at early postoperative stages may predict chronic (neuropathic) pain after surgery. Currently available animal models are typically associated with consistent tactile hypersensitivity and are therefore limited to distinguish between mechanisms that underlie tactile hypersensitivity as opposed to mechanisms that protect against it. In this study we have modified the rat model of spared nerve injury, restricting the surgical lesion to a single peripheral branch of the sciatic nerve. This modification reduced the prevalence of tactile hypersensitivity from nearly 100% to approximately 50%. With this model, we here also demonstrated that the Regulator of G protein Signaling 4 (RGS4) was specifically up-regulated in the lumbar dorsal root ganglia and dorsal horn of rats developing tactile hypersensitivity. Intrathecal delivery of the RGS4 inhibitor CCG63802 was found to reverse tactile hypersensitivity for a 1h period. Moreover, tactile hypersensitivity after modified spared nerve injury was most frequently persistent for at least four weeks and associated with higher reactivity of glial cells in the lumbar dorsal horn. Based on these data we suggest that this new animal model of nerve injury represents an asset in understanding divergent neuropathic pain outcomes, so far unravelling a role of RGS4 in tactile hypersensitivity. Whether this model also holds promise in the study of the transition from acute to chronic pain will have to be seen in future investigations.Copyright © 2016. Published by Elsevier Inc.

57 keywords...

hide…