Behavioral and immunohistological assessment of painful neuropathy induced by a single oxaliplatin injection in the rat

Ling, Bing; Coudoré-Civiale, Marie-Ange; Balayssac, David; Eschalier, Alain; François, Clément; Authier, Nicolas

doi:10.1016/j.tox.2007.02.013

Cited by 88 publications

(104 citation statements)

References 32 publications

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“…The acute syndrome, characterised by distal dyasthesias, generally resolves within days of treatment completion, while a more chronic syndrome occurs in 10-20% of patients (Park et al 2008). Similar results have been found in rodents (Cavaletti et al 2001; Ling et al 2007). This research has shown that sensory neuronal bodies in the dorsal root ganglion are vulnerable to damage, and changes in voltage-gated Na + channel function of motor axons are associated with the development of chronic neuropathy (Park et al 2008).…”

Section: Discussionsupporting

confidence: 71%

“…The OX dose was chosen to reflect clinically equivalent cumulative dose and based on the work of Ling and colleagues who found a single i.p. injection of 12 mg/kg OX-induced peripheral neuropathies similar to those experienced by patients receiving oxaliplatin chemotherapy (Ling et al 2007). Pilot studies (data not shown) confirmed that these doses produced measurable cognitive impairments.…”

Section: Drug Administrationmentioning

confidence: 69%

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Cognitive impairments caused by oxaliplatin and 5-fluorouracil chemotherapy are ameliorated by physical activity

et al. 2011

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Section: Discussionsupporting

confidence: 71%

Section: Drug Administrationmentioning

confidence: 69%

Cognitive impairments caused by oxaliplatin and 5-fluorouracil chemotherapy are ameliorated by physical activity

et al. 2011

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“…Oxaliplatin Administration Oxaliplatin was obtained from Sigma Chemical Co., U.S.A. As described previously, 6,22) oxaliplatin was dissolved in a 5% glucose solution at a concentration of 2 mg/mL and was intraperitoneally administered at 6 mg/kg.…”

Section: )mentioning

confidence: 99%

Nicotinic Acetylcholine Receptors Mediate the Suppressive Effect of an Injection of Diluted Bee Venom into the GV3 Acupoint on Oxaliplatin-Induced Neuropathic Cold Allodynia in Rats

Yoon

Kim

Yoon

et al. 2015

Biological & Pharmaceutical Bulletin

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Oxaliplatin, a platinum-based chemotherapy drug, often induces acute neuropathic pain, especially cold allodynia, even after a single administration. Subcutaneous injection of diluted bee venom (BV) into acupoints has been used to treat various pain symptoms in traditional oriental medicine. Although we previously demonstrated the suppressive effect of BV injection on oxaliplatin-induced cold allodynia in rats, its neurochemical mechanism remained unclear. This study investigates whether and how the cholinergic system mediates the relieving effect of BV injection on cold allodynia in oxaliplatin-administered rats. The behavioral signs of cold allodynia induced by an oxaliplatin administration (6 mg/kg, intraperitoneally (i.p.)) were evaluated by a tail immersion test in cold water (4°C). BV (0.25 mg/kg, subcutaneously (s.c.)) injection into the Yaoyangguan acupoint, located between the spinous processes of the fourth and fifth lumbar vertebrae, significantly alleviated the cold allodynia. This relieving effect of BV injection on oxaliplatin-induced cold allodynia was blocked by a pretreatment with mecamylamine (a non-selective nicotinic receptor antagonist, 2 mg/kg, i.p.), but not by atropine (a non-selective muscarinic receptor antagonist, 1 mg/kg, i.p.). Further, dihydro-β-erythroidinehydrobromide (DHβE, an α4β2 nicotinic antagonist, 5 mg/kg, i.p.) prevented the antiallodynic effect of BV, whereas methyllycaconitine (an α7 nicotinic antagonist, 6 mg/kg, i.p.) did not. Finally, intrathecal administration of DHβE (10 nM) blocked the BV-induced anti-allodynic effect. These results suggest that nicotinic acetylcholine receptors, especially spinal α4β2 receptors, but not muscarinic receptors, mediate the suppressive effect of BV injection on oxaliplatin-induced acute cold allodynia in rats.Key words oxaliplatin; bee venom; cholinergic; cold allodynia; nicotinic receptor; rat Oxaliplatin is a third-generation platinum-based chemotherapy drug for advanced colorectal cancer.1) Unlike the other platinum compounds (e.g. cisplatin and carboplatin), oxaliplatin does not induce nephrotoxicity and hepatotoxicity, but often induces a very acute painful neuropathy soon after an administration.2) This acute neuropathy is the only major dose-limiting toxicity associated with oxaliplatin use 3) and is characterized by the rapid onset of cold-induced peripheral dysesthesia, paresthesia, or hypoesthesia of the hands, feet, or throat. 4,5) Previous animal studies also have shown that a single administration of oxaliplatin (6 mg/kg, intraperitoneally (i.p.)) reproduces the neurotoxic profile, especially cold allodynia.6,7) However, its mechanism is still unclear and an effective treatment of established neuropathic cold allodynia remains to be found. 8)A subcutaneous injection of diluted bee venom (BV) into acupoints, so called 'bee venom acupuncture,' has been used as a part of traditional oriental medicine to relieve pain and treat various diseases, such as arthritis, rheumatism, cancer, asthma and skin diseases.9-11) It is a kind...

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“…An immunohistochemical study in the superficial layers of the spinal dorsal horn revealed a marked increase in substance P immunoreactivity. 41 Another acute model has been published by Joseph et al, 42 also displaying a dose-dependent heat and cold allodynia with a mechanical hyperalgesia. They also assessed different inhibitors of several second messengers (protein kinase A, protein kinase C, NO, Ca 2ϩ , Caspase), which failed to attenuate the acute mechanical hyperalgesia, whereas antioxydants (acetyl-L-carnitine, ␣-lipoic acid, vitamin C) and inhibitors of the mitochondrial electron transport chain (rotenone, 3-nitropropionic acid, antimycin, sodium cyanide, oligomycin) produced significant attenuation.…”

Section: Platinum Compoundsmentioning

confidence: 99%

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

et al. 2009

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Summary:This review examines recent preclinical research on toxic peripheral neuropathy and potential therapeutic developments. Chemotherapy-induced peripheral neurotoxicity is a major clinical problem because it represents the dose-limiting side effects of a significant number of antineoplastic drugs. Patients are unable to complete full or optimal treatment schedules. The incidence of chemotherapy-induced peripheral neuropathy varies depending on the drugs and schedules used, and this can be quite high, particularly when neurophysiological methods are used to make a diagnosis. However, even when chemotherapy-induced peripheral neuropathy is not a doselimiting side effect, its onset may severely affect the quality of life of cancer patients and cause chronic discomfort. As such, improved understanding of the pathophysiology of chemotherapy-induced neurotoxicity need for animal models is clinically relevant and will assist in the development of future neuroprotective strategies and also in the design of novel chemotherapies with improved toxicity profiles. In this review, the features of animal models of chemotherapy-induced painful neuropathy developed for 20 years, due to the administration of the most widely used drugs, such as platinum drugs, taxanes, and vinca alkaloids, will be discussed. In a second part, data available on neuroprotectants and treatment strategies, evaluated using these previous animal models in the attempt to prevent neuropathic pain, will be summarized.

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Behavioral and immunohistological assessment of painful neuropathy induced by a single oxaliplatin injection in the rat

Cited by 88 publications

References 32 publications

Cognitive impairments caused by oxaliplatin and 5-fluorouracil chemotherapy are ameliorated by physical activity

Cognitive impairments caused by oxaliplatin and 5-fluorouracil chemotherapy are ameliorated by physical activity

Nicotinic Acetylcholine Receptors Mediate the Suppressive Effect of an Injection of Diluted Bee Venom into the GV3 Acupoint on Oxaliplatin-Induced Neuropathic Cold Allodynia in Rats

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

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