Journal
NEUROSCIENCE LETTERS
Volume 465, Issue 2, Pages 184-188Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2009.08.063
Keywords
Joint pain; Osteoarthritis; Monosodium iodoacetate; Electrophysiological recordings; Animal model; Joint primary afferents
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Funding
- Alberta Heritage Foundation for Medical Research (AHFMR)
- Arthritis Society of Canada
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Osteoarthritis (OA) is a degenerative joint disease characterized by joint pain for which there is currently no effective treatment. Previous studies have found that intra-articular injection of monosodium iodoacetate (MIA) caused a dose-dependent destruction of rat knees with concomitant increased pain. In this study, varying degrees of OA were induced by intra-articular injection of 0.1 mg, 0.3 mg and 3 mg MIA. Electrophysiological recordings were made from knee joint primary afferents in response to rotation of the joint and firing frequencies were determined and compared to saline-injected control joints. The analgesic effect of local application of the classic non-steroidal anti-inflammatory drug (NSAID) diclofenac (0.1 mg/0.1 ml bolus) was also determined in each group. Joint afferent firing frequency was significantly enhanced in OA knees compared to saline injected control joints and the magnitude of this sensitization showed a direct relationship with increasing dose of MIA. Diclofenac reduced nociception significantly in the 3 mg MIA treated joint, but had no effect on nerve mechanosensitivity in rats with milder OA. This study shows for the first time that MIA produces a graded sensitization of joint nociceptors making this a useful model for the study of pain mechanisms in joints with progressive CA severity. The anti-nociceptive effect of diclofenac further indicates that the MIA model offers an attractive means of objectively testing potential therapeutic agents (c) 2009 Elsevier Ireland Ltd. All rights reserved.
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