Intrathecally administered endotoxin or cytokines produce allodynia, hyperalgesia and changes in spinal cord neuronal responses to nociceptive stimuli in the rat

• DOI: 10.1053/eujp.2000.0177
• Publication Date: 2002-09-19T13:56:27Z
• Authors: Alison J. Reeve; Sadhana Patel; Alyson Fox; Katherine Walker; Laszlo Urban
• Keywords: Allodynia

Inflammatory processes occurring within the central nervous system (CNS) can produce 'illness induced behaviours' which include fever, sleep and development of allodynia hyperalgesia. Here we demonstrate effects pro-inflammatory mediators, bacterial endotoxin, rat recombinant interleukin 1 beta (rrIL-1 beta) or tumour necrosis factor-alpha (rrTNF alpha) on integration somatosensory information at single neuronal level, via recordings from wide-dynamic range neurones in dorsal horn spinal cord anaesthetized rats. Intrathecal administration E. coli lipopolysaccharide (LPS, 10 100 microg, i.t.) enhanced activity neurones, including facilitation post-discharge. IL-1 (5-5000 pg) TNF-alpha responses, acute responses to C-fibre stimulation, wind-up post-discharge, however, were more robust than those TNF alpha. (1-1000 also leads mechanical On other hand intrathecal application alpha did not changes sensitivity stimuli. Changes by local inflammation may provide a pathomechanism for clinical pathology pain syndrome, accompany CNS disease injury.