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Pain. 2006 Dec 15;126(1-3):280-93. Epub 2006 Aug 30.

Spinal pathways involved in supraspinal modulation of neuropathic manifestations in rats.

Author information

1
Department of Human Morphology, Faculty of Medicine, American University of Beirut, Beirut, Lebanon. nesaade@aub.edu.lb

Abstract

Controversial results have been recently reported on the role of supraspinal centers in the modulation of nociceptive behavior in animal models of mononeuropathy. Our aim was to investigate the role of the various spinal pathways in the modulation of the neuropathic manifestations. Several groups of rats were subjected to selective spinal-tract lesions, either 2-3 weeks before or 2-3 weeks after the induction of mononeuropathy following the chronic constriction injury (CCI) or the spared nerve injury (SNI) models. Tactile and cold allodynias were assessed by Von Frey filaments and the acetone drops test, respectively. Thermal hyperalgesia was assessed by the paw withdrawal and the hot plate tests. The effects of unilateral and bilateral lesions of the dorso-lateral funiculus (DLF), the anterolateral column (ALC) or hemisection were tested over a period of 4-8 weeks. All spinal tract lesions produced reversible, but significant decrease of allodynia and hyperalgesia over a period of 1-3 weeks. The most pronounced effects were observed with bilateral lesions. The stronger attenuation was observed on thermal hyperalgesia, assessed by the paw withdrawal test, while cold allodynia was the least affected. Spinal lesions performed before the induction of neuropathy did not produce significant alterations in the temporal development of neuropathic manifestations. The present results allow the conclusion that all spinal tracts can be involved in the rostral transmission and the descending modulation of neuropathic manifestations. The recovery of symptoms following spinal lesions provides illustration on the plasticity of the neural network involved in the processing of the neuropathic syndromes.

PMID:
16945485
DOI:
10.1016/j.pain.2006.07.010
[Indexed for MEDLINE]

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