Spinal nociceptive reflexes are sensitized in the monosodium iodoacetate model of osteoarthritis pain in the rat

Kelly, Sara; Dobson, Katharine L.; Harris, J.

doi:10.1016/j.joca.2013.07.002

Cited by 36 publications

(36 citation statements)

References 41 publications

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“…Recent studies have advanced understanding of the spinal mechanisms contributing to OA pain behaviour, demonstrating important contributions of dorsal horn neuronal excitability (Sagar et al, ; Kelly et al, ) and activation of spinal glia cells (Lee et al, ; Sagar et al, ; Ogbonna et al, ; Yu et al, ) (see references in Rani Sagar et al, ). In the present study, repeated MJN110 treatment did not significantly inhibit MIA‐induced increases in GFAP mRNA in the dorsal horn of the spinal cord, which contrasts with the reported effects of an exogenous cannabinoid ligand selective for the CB 2 receptor (Burston et al, ).…”

Section: Discussionmentioning

confidence: 99%

Robust anti‐nociceptive effects of monoacylglycerol lipase inhibition in a model of osteoarthritis pain

Burston

Mapp

Sarmad

et al. 2016

British J Pharmacology

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BACKGROUND AND PURPOSEChronic pain is often a symptom of knee osteoarthritis (OA) for which current analgesics are either inadequate or are associated with serious side effects. The endocannabinoid system may offer alternative targets for pain relief. We evaluated the effects of a potent and selective monoacylglycerol (MAG) lipase inhibitor (MJN110) on OA pain behaviour, spinal mechanisms of action and joint histopathology in the rat. EXPERIMENTAL APPROACHIntra-articular injection of monosodium iodoacetate (MIA) models OA pain and mimics clinical joint pathology. Effects of MJN110 on MIA-induced weight-bearing asymmetry and lowered paw withdrawal thresholds (PWTs), changes in spinal gene expression and brain levels of relevant lipids were determined. KEY RESULTSAcute MJN110 (5 mg·kg À1 ) significantly reversed MIA-induced weight-bearing asymmetry (MIA/vehicle: 68 ± 6 g; MIA/MJN110: 35 ± 4 g) and lowered ipsilateral PWTs (MIA/vehicle: 7 ± 0.8 g; MIA/MJN110: 11 ± 0.6 g), via both CB 1 and CB 2 receptors. Repeated treatment with MJN110 (5 mg·kg À1 ) resulted in anti-nociceptive tolerance. A lower dose of MJN110 (1 mg·kg À1 ) acutely inhibited pain behaviour, which was maintained for 1 week of repeated administration but had no effect on joint histology. MJN110 significantly inhibited expression of membrane-associated PGE synthase-1 in the ipsilateral dorsal horn of the spinal cord of MIA rats, compared with vehicle-treated MIA rats. Both doses of MJN110 significantly elevated brain levels of the endocannabinoid 2-arachidonoylglycerol. CONCLUSIONS AND IMPLICATIONSOur data support further assessment of the therapeutic potential of MAG lipase inhibitors for the treatment of OA pain. Abbreviations

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Section: Discussionmentioning

confidence: 99%

Robust anti‐nociceptive effects of monoacylglycerol lipase inhibition in a model of osteoarthritis pain

Burston

Mapp

Sarmad

et al. 2016

British J Pharmacology

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“…These are accompanied by changes in the expression of pain-mediating cytokines in the DRG and spinal cord which correlate with the development of hyperalgesia and allodynia (Im et al, 2010). The same model causes reduced nociceptive thresholds in the biceps femoris which neurophysiologically represents a spinal mechanism (Kelly et al, 2013). The monoiodoacetate (MIA) model also seems capable of activating spinal glial cells which may contribute to the development and maintenance of CS (Sagar et al, 2011).…”

Section: Osteoarthritis (Oa) Painmentioning

confidence: 99%

Assessment and manifestation of central sensitisation across different chronic pain conditions

Arendt-Nielsen

Morlion

Perrot

et al. 2017

European Journal of Pain

517

494

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Different neuroplastic processes can occur along the nociceptive pathways and may be important in the transition from acute to chronic pain and for diagnosis and development of optimal management strategies. The neuroplastic processes may result in gain (sensitisation) or loss (desensitisation) of function in relation to the incoming nociceptive signals. Such processes play important roles in chronic pain, and although the clinical manifestations differ across condition processes, they share some common mechanistic features. The fundamental understanding and quantitative assessment of particularly some of the central sensitisation mechanisms can be translated from preclinical studies into the clinic. The clinical perspectives are implementation of such novel information into diagnostics, mechanistic phenotyping, prevention, personalised treatment, and drug development. The aims of this paper are to introduce and discuss (1) some common fundamental central pain mechanisms, (2) how they may translate into the clinical signs and symptoms across different chronic pain conditions, (3) how to evaluate gain and loss of function using quantitative pain assessment tools, and (4) the implications for optimising prevention and management of pain. The chronic pain conditions selected for the paper are neuropathic pain in general, musculoskeletal pain (chronic low back pain and osteoarthritic pain in particular), and visceral pain (irritable bowel syndrome in particular). The translational mechanisms addressed are local and widespread sensitisation, central summation, and descending pain modulation. Significance Central sensitisation is an important manifestation involved in many different chronic pain conditions. Central sensitisation can be different to assess and evaluate as the manifestations vary from pain condition to pain condition. Understanding central sensitisation may promote better profiling and diagnosis of pain patients and development of new regimes for mechanism based therapy. Some of the mechanisms underlying central sensitisation can be translated from animals to humans providing new options in development of therapies and profiling drugs under development.

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“…CZ extract increased the induction of HO-1 and inhibited IL-1β, IL-6, and cyclooxygenase-2 mRNA levels in LPS-stimulated RAW264.7 cells. 12,25) Recently, Kim et al reported that extract from CZ ameliorated arthritis symptoms and bone erosion in collageninduced rheumatoid arthritis. 17) Here, we demonstrated the protective effect of BST106 against OA-related cartilage damage.…”

Section: Discussionmentioning

confidence: 99%

BST106 Protects against Cartilage Damage by Inhibition of Apoptosis and Enhancement of Autophagy in Osteoarthritic Rats

Hong

Shin

Kim

et al. 2018

Biological & Pharmaceutical Bulletin

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Chrysanthemum zawadskii var. latilobum (CZ) has been used as a traditional medicine in Asian countries for the treatment of inflammatory diseases. Recently, CZ extract was shown to inhibit differentiation of osteoclasts and provide protection against rheumatoid arthritis. The aim of this study was to investigate the molecular mechanisms of BST106, the ethanol extract of CZ, for cartilage protection in monosodium iodoacetate (MIA)-induced osteoarthritis (OA), particularly focusing on apoptosis and autophagy. BST106 (50, 100, and 200 mg/kg) was orally administered once daily to MIA-induced OA rats. Swelling, limping, roentgenography, and histomorphological changes were assessed 28 d after MIA injection. Biochemical parameters for matrix metalloproteinase (MMP), apoptosis, and autophagy were also assessed. BST106 ameliorated the severity of swelling and limping after MIA injection. Roentgenographic and histomorphological examinations revealed that BST106 reduced MIA-induced cartilage damage. BST106 decreased MIA-induced increases in MMP-2 and MMP-13 mRNA levels. Increased levels of serum cartilage oligomeric matrix protein and glycosaminoglycan release were attenuated by BST106. Furthermore, BST106 suppressed the protein expression of proapoptotic molecules and increased the protein expression of autophagosome- and autolysosome-related molecules. These findings indicate that BST106 protects against OA-induced cartilage damage by inhibition of the apoptotic pathway and restoration of impaired autophagic flux.

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Spinal nociceptive reflexes are sensitized in the monosodium iodoacetate model of osteoarthritis pain in the rat

Cited by 36 publications

References 41 publications

Robust anti‐nociceptive effects of monoacylglycerol lipase inhibition in a model of osteoarthritis pain

Robust anti‐nociceptive effects of monoacylglycerol lipase inhibition in a model of osteoarthritis pain

Assessment and manifestation of central sensitisation across different chronic pain conditions

BST106 Protects against Cartilage Damage by Inhibition of Apoptosis and Enhancement of Autophagy in Osteoarthritic Rats

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