Involvement of increased expression of transient receptor potential melastatin 8 in oxaliplatin-induced cold allodynia in mice

Gauchan, Punam; Andoh, Tsugunobu; Kato, Atsushi; Kuraishi, Yasushi

doi:10.1016/j.neulet.2009.04.029

Cited by 148 publications

(153 citation statements)

References 23 publications

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“…Artemin-and NGF-induced sensitization of cold responses is TRPM8-dependent, and multiple studies have shown that TRPM8 plays a role in the development of cold allodynia (8,(22)(23)(24)57). However, inflammatory cold allodynia is also diminished by both an TRPA1 antagonist and reduced TRPA1 transcript expression, and cold hypersensitivity can be induced by TRPA1 agonism in WT but not Trpa1 −/− mice (58, 59).…”

Section: Discussionmentioning

confidence: 99%

Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3

Lippoldt

Ongun

Kusaka

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Tissue injury prompts the release of a number of proalgesic molecules that induce acute and chronic pain by sensitizing pain-sensing neurons (nociceptors) to heat and mechanical stimuli. In contrast, many proalgesics have no effect on cold sensitivity or can inhibit cold-sensitive neurons and diminish cooling-mediated pain relief (analgesia). Nonetheless, cold pain (allodynia) is prevalent in many inflammatory and neuropathic pain settings, with little known of the mechanisms promoting pain vs. those dampening analgesia. Here, we show that cold allodynia induced by inflammation, nerve injury, and chemotherapeutics is abolished in mice lacking the neurotrophic factor receptor glial cell line-derived neurotrophic factor family of receptors-α3 (GFRα3). Furthermore, established cold allodynia is blocked in animals treated with neutralizing antibodies against the GFRα3 ligand, artemin. In contrast, heat and mechanical pain are unchanged, and results show that, in striking contrast to the redundant mechanisms sensitizing other modalities after an insult, cold allodynia is mediated exclusively by a single molecular pathway, suggesting that artemin-GFRα3 signaling can be targeted to selectively treat cold pain.W hen pain continues past its usefulness as a warning of potential tissue damage, it becomes a debilitating condition for which few viable treatments are currently available. The result can be an exacerbation of pain in response to both innocuous (allodynia) and noxious (hyperalgesia) stimuli (1). For example, pain felt with normally pleasant mild cooling (cold allodynia) occurs in many pathological conditions, such as fibromyalgia, multiple sclerosis, stroke, and chemotherapeutic-induced polyneuropathy, but what underlies this specific form of pain at the cellular or molecular level is largely unknown (2-5). Pain-sensing afferent neurons (nociceptors) are sensitized during injury or disease, in part, by a vast array of proalgesic compounds termed the "inflammatory soup" (e.g., neurotrophic factors, protons, bradykinin, prostaglandins, and ATP) (1). These substances are released locally at the site of injury by infiltrating immune cells, such as macrophages, neutrophils, and T cells, as well as resident cells, including keratinocytes and mast cells (6), and either directly activate sensory receptors or sensitize them to subsequent stimuli (7). Moreover, prolonged inflammation can lead to central sensitization (in the spinal cord and brain) and bring about long-lasting chronic pain that persists after acute inflammation has resolved. Thus, a better understanding of the molecules involved in neuroinflammation may lead to therapeutic options for acute and chronic pain.Of the range of proalgesics known to promote pain, only nerve growth factor (NGF) and the glial cell line-derived neurotrophic factor family ligand (GFL) artemin have been shown to lead to cold hypersensitivity (8-11). Both are major components of the inflammatory soup and produce nociceptor sensitization and pain through their cognate cell surface rece...

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Section: Discussionmentioning

confidence: 99%

Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3

Lippoldt

Ongun

Kusaka

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…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. 43 Very recently, mice models have also been published, using single 26,44 or repeated administrations, 44 respectively, showing significant mechanical and cold allodynia and hyperalgesia. Gauchan et al 44 also demonstrated that oxaliplatin-induced cold allodynia could be partly explained by an increase in the expression level of TRPM8 mRNA at day 3 after a single injection.…”

Section: Platinum Compoundsmentioning

confidence: 99%

“…43 Very recently, mice models have also been published, using single 26,44 or repeated administrations, 44 respectively, showing significant mechanical and cold allodynia and hyperalgesia. Gauchan et al 44 also demonstrated that oxaliplatin-induced cold allodynia could be partly explained by an increase in the expression level of TRPM8 mRNA at day 3 after a single injection.…”

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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“…An increase in TRPM8 expression occurs in some sensory neurons after nerve injury [150], possibly contributing to enhanced cooling sensation. Similarly, oxaliplatin increased the expression of TRPM8 mRNA in mouse DRG neurons when cold hypersensitivity peaked, suggesting that cold hypersensitivity is, at least partly, due to the increased expression of TRPM8 in primary sensory neurons [151]. In addition, wet-dog shake and jumping behaviors elicited by icilin, a non selective TRPM8 activator, were significantly increased in mice treated with oxaliplatin [151].…”

Section: Trpm8mentioning

confidence: 93%

“…Similarly, oxaliplatin increased the expression of TRPM8 mRNA in mouse DRG neurons when cold hypersensitivity peaked, suggesting that cold hypersensitivity is, at least partly, due to the increased expression of TRPM8 in primary sensory neurons [151]. In addition, wet-dog shake and jumping behaviors elicited by icilin, a non selective TRPM8 activator, were significantly increased in mice treated with oxaliplatin [151]. Oxaliplatin seems to affect TRPA1 rather than TRPM8, because oxaliplatin-treatment induces sensitization to icilin, which also activates TRPA1 expressing neurons, but not the response to a TRPM8 selective ligand, WS12 [81].…”

Section: Trpm8mentioning

confidence: 95%

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

Nassini¹,

Benemei²,

Fusi³

et al. 2013

TOPAINJ

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Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a common dose-limiting side effect of many chemotherapeutic drugs, including platinum-based compounds (e.g., cisplatin and oxaliplatin), taxanes (e.g., paclitaxel), vinca alkaloids (e.g., vincristine), and the first-in-class proteasome inhibitor, bortezomib. Among the various sensory symptoms of CIPN, paresthesia, dysesthesia, spontaneous pain, and mechanical and thermal hypersensitivity are prominent. Inflammation, oxidative stress, loss of intraepidermal nerve fibers, modifications of mitochondria, and various ion channels alterations are part of the several mechanisms contributing to CIPN. Because attempts to mitigate chemotherapeutic-induced acute neuronal hyperexcitability and the subsequent peripheral neuropathy have yielded unsatisfactory results, a more in-depth understanding of the mechanism(s) responsible for the neurotoxic action of anticancer drugs is required.Some members of the transient receptor potential (TRP) family of channels, as the TRPV1 and TRPV4 (vanilloid), TRPA1 (ankyrin) and TRPM8 (melastatin) are expressed on the plasma membrane of primary sensory neurons (nociceptors), where they are activated by an unprecedented series of physical and chemical stimuli. There is evidence that TRPV1, TRPV4, TRPA1 and TRPM8 are prominent contributors of mechanical and thermal hypersensitivity in models of CIPN. In particular, in vitro and in vivo studies have pointed out the unique role of TRPA1 and oxidative stress in the mechanism responsible for cold and mechanical hyperalgesia in rodent models of CIPN.

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Involvement of increased expression of transient receptor potential melastatin 8 in oxaliplatin-induced cold allodynia in mice

Cited by 148 publications

References 23 publications

Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3

Inflammatory and neuropathic cold allodynia are selectively mediated by the neurotrophic factor receptor GFRα3

Animal Models of Chemotherapy-Evoked Painful Peripheral Neuropathies

Transient Receptor Potential Channels in Chemotherapy-Induced Neuropathy

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