Differential expression of Cathepsin S and X in the spinal cord of a rat neuropathic pain model

• Published in: BMC neuroscience 2008-08, Vol.9 (1), p.80-80, Article 80
• Main Authors: Leichsenring, Anna, Bäcker, Ingo, Wendt, Wiebke, Andriske, Michael, Schmitz, Beate, Stichel, Christine C, Lübbert, Hermann
• Format: Article
• Language: English
• Subjects: Animals; Cathepsin K; Cathepsins; Cathepsins - biosynthesis; Cathepsins - genetics; Chronic pain; Diagnosis; Disease Models, Animal; Gene Expression Regulation - physiology; Male; Neuralgia - enzymology; Neuralgia - genetics; Neuralgia - pathology; Pain Measurement - methods; Physiological aspects; Rats; Rats, Wistar; Risk factors; Spinal cord; Spinal Cord - enzymology; Spinal Cord - pathology
• ISSN: 1471-2202; 1471-2202
• DOI: 10.1186/1471-2202-9-80

Ample evidence suggests a substantial contribution of cellular and molecular changes in the spinal cord to the induction and persistence of chronic neuropathic pain conditions. While for a long time, proteases were mainly considered as protein degrading enzymes, they are now receiving growing interest as signalling molecules in the pain pathology. In the present study we focused on two cathepsins, CATS and CATX, and studied their spatiotemporal expression and activity during the development and progression of neuropathic pain in the CNS of the rat 5th lumbar spinal nerve transection model (L5T). Immediately after the lesion, both cathepsins, CATS and CATX, were upregulated in the spinal cord. Moreover, we succeeded in measuring the activity of CATX, which was substantially increased after L5T. The differential expression of these proteins exhibited the same spatial distribution and temporal progression in the spinal cord, progressing up to the medulla oblongata in the late phase of chronic pain. The cellular distribution of CATS and CATX was, however, considerably different. The cellular distribution and the spatio-temporal development of the altered expression of CATS and CATX suggest that these proteins are important players in the spinal mechanisms involved in chronic pain induction and maintenance.