Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats

Nagakura, Yukinori; Takahashi, M; Noto, Takahisa; Sekizawa, Tsuyoshi; Oe, Tomoya; Yoshimi, Eiji; Tamaki, Keisuke; Shimizu, Yoshiyuki

doi:10.1016/j.bbr.2011.09.023

Cited by 39 publications

(38 citation statements)

References 43 publications

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“…This pattern of altered mechanical sensitivity combined with a reduced number of mechanoresponsive unmyelinated C-fibers is also observed in aging 28,29,51,53 and diabetic neuropathy, 18,36 and may also correspond with reports of small-fiber polyneuropathy in some patients diagnosed with fibromyalgia 32 and restless legs syndrome. 38 These changes seem to be related with decreased neurotrophic factors in primary sensory neurons, 3,18 however, in a reserpine-induced pain model, no apparent histological changes were detected in the sciatic nerve bundle and DRG by light microscopy, 27 which suggests that this paradoxical change in mechanical sensitivity likely results from reserpine-mediated functional alterations in the peripheral nervous system.…”

Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 98%

“…This hypothesis is supported by a previous report that showed no apparent histological change in DRG. 27 For further confirmation of the integrity of the sciatic nerve bundle, electron microscopic observation will be required.…”

Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 99%

“…26 In the peripheral nervous system, reserpine has been shown to deplete monoamines, 1 although no degeneration was recognized in the sciatic nerve or dorsal root ganglion (DRG). 27 Potential consequences of peripheral monoamine depletion are unknown, although neuromodulatory effects of these transmitters on nociceptors are well described. 12,23,24 Under hyperalgesic conditions, such as inflammation and neuropathy, many ion channels that are responsible for pain, mechanotransduction, and generation/propagation of action Sponsorships or competing interests that may be relevant to content are disclosed at the end of this article.…”

Section: Introductionmentioning

confidence: 99%

“…16 However, alterations in the peripheral afferents and spinal cord have not been examined in a reserpine-induced pain model, and different pathological mechanisms have been suggested in its etiology. 27 This study aimed to clarify the peripheral and spinal mechanisms of nociception and pain in a reserpine-induced pain model by analyzing the following: (1) expression of ion channels that are responsible for pain, mechanotransduction, and the generation and propagation of action potentials in the DRG, (2) axonal conductive and receptive properties of peripheral nociceptive afferents, and (3) alterations in spinal microglial cells. A preliminary account of this research previously appeared in an abstract form.…”

Section: Introductionmentioning

confidence: 99%

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Peripheral and spinal mechanisms of nociception in a rat reserpine-induced pain model

Taguchi

Katanosaka

Yasui

et al. 2015

Pain

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Chronic widespread pain is a serious medical problem, yet the mechanisms of nociception and pain are poorly understood. Using a reserpine-induced pain model originally reported as a putative animal model for fibromyalgia, this study was undertaken to examine the following: (1) expression of several ion channels responsible for pain, mechanotransduction, and generation/propagation of action potentials in the dorsal root ganglion (DRG), (2) activities of peripheral nociceptive afferents, and (3) alterations in spinal microglial cells. A significant increase in mRNA expression of the acid-sensing ion channel (ASIC)-3 was detected in the DRG, and the behavioral mechanical hyperalgesia was significantly reversed by subcutaneous injection of APETx2, a selective blocker of ASIC3. Single-fiber recordings in vitro revealed facilitated mechanical responses of mechanoresponsive C-fibers both in the skin and muscle although the proportion of mechanoresponsive C-nociceptors was paradoxically decreased. In the spinal dorsal horn, microglial cells labeled with Iba1 immunoreactivity was activated, especially in laminae I-II where the nociceptive input is mainly processed compared with the other laminae. The activated microglia and behavioral hyperalgesia were significantly tranquilized by intraperitoneal injection of minocycline. These results suggest that the increase in ASIC3 in the DRG facilitated mechanical response of the remaining C-nociceptors and that activated spinal microglia may direct to intensify pain in this model. Pain may be further amplified by reserpine-induced dysfunction of the descending pain inhibitory system and by the decrease in peripheral drive to this system resulting from a reduced proportion of mechanoresponsive C-nociceptors.

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Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 98%

Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Peripheral and spinal mechanisms of nociception in a rat reserpine-induced pain model

Taguchi

Katanosaka

Yasui

et al. 2015

Pain

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“…However, in spite of its name, at the histological level, FM does not show any fibrosis. In FM, which affects 2–4% of the population, mostly women, there is an increase in reactivity of central neurons with increased sensitivity localized mainly in the central nervous system (CNS) (Nagakura et al, ). It is a chronic, idiopathic disorder, which affects about 12 million people in the United States, and is probably due to an interaction between the sympathetic nervous system, neurotransmitters, external stressor, and/or hormones (Zhang, Wang, Fu, & Yan, ).…”

Section: Introductionmentioning

confidence: 99%

Impact of mast cells in fibromyalgia and low‐grade chronic inflammation: Can IL‐37 play a role?

Conti

Gallenga

Caraffa

et al. 2019

Dermatologic Therapy

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Fibromyalgia (FM) is a disease characterized by chronic widespread pain, fatigue, aches, joint stiffness, depression, cognitive dysfunction, and nonrestorative sleep. In FM, neurotransmission and glial activation can occur with an increase in inflammatory cytokines and involvement of mast cells (MCs) in the skin. FM skin biopsiesshow an increase in the number of MCs, as well as the production of corticotropin releasing hormone and substance P (SP) by the neurons, which in turn activate MCs to release neurosensitizing proinflammatory substances, such as cytokines, secreted preformed mediators, and lipids, which can exacerbate low-grade inflammation. In fact, certain proinflammatory cytokines are higher in FM and mediate muscle pain, the mechanism of which is not yet clear. MC-derived tumor necrosis factor (TNF) induces nerve growth factor (NGF) and participates in nerve fiber elongation in skin hypersensitivity. IL-37 is an inhibitor of proinflammatory IL-1 family members, which are generated and released by MCs. The goal of this article is to demonstrate that inflammatory cytokines and MC products play a role in FM and that inflammation may be inhibited by IL-37. Here, we propose IL-37 as a cytokine that contributes to improve the pathogenesis of FM by blocking IL-1 family members.

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Ferulic acid increases pain threshold and ameliorates depression-like behaviors in reserpine-treated mice: behavioral and neurobiological analyses

Zhang

Shao

et al. 2013

Metab Brain Dis

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Depression-pain dyad involves a series of pathological changes including the dysfunction of neuroendocrine and immune networks. Depression and pain influence each other, but the mechanisms are still obscure. The present study aimed to investigate the effect of ferulic acid (FA) on reserpine-induced pain and depression-like behaviors in mice. The results showed that reserpine (1 mg/kg for 3 days, i.p.) led to a significant decrease in nociceptive threshold in thermal hyperalgesia and mechanical allodynia, as well as a significant increase in the immobility time in mouse models of despair test. The neurochemical assays suggested the decreased neurotransmitters (dopamine, norepinephrine and serotonin) along with the increased oxidative stress, inflammatory cytokines, and apoptotic parameters in the frontal cortex and hippocampus of the reserpinised mice. Treatment with FA (40 or 80 mg/kg, p.o.) reversed the behavioral abnormalities and decreased norepinephrine, serotonin and dopamine levels in the hippocampus and frontal cortex induced by reserpine. The higher dose of FA effectively antagonized the oxidative and nitrosative stress and inflammation as evidenced by down-regulated nitrite, LPO, IL-1β, TNF-α, and up-regulated GSH and SOD. Furthermore, FA produced a dose dependent decrease in substance P, NF-κβ p65 and caspase-3 levels in the frontal cortex and hippocampus of reserpinised mice. The findings suggest that FA exerts the effects on reserpine-induced pain and depression-like behaviors through regulating monoaminergic system, oxidative/antioxidant defense, inflammatory and apoptotic signaling pathways. Understanding the mechanism by which FA ameliorates depression and pain as a multi-targeted compound could open new avenues for the development of innovative treatments for depression coupled with pain.

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Different pathophysiology underlying animal models of fibromyalgia and neuropathic pain: Comparison of reserpine-induced myalgia and chronic constriction injury rats

Cited by 39 publications

References 43 publications

Peripheral and spinal mechanisms of nociception in a rat reserpine-induced pain model

Peripheral and spinal mechanisms of nociception in a rat reserpine-induced pain model

Impact of mast cells in fibromyalgia and low‐grade chronic inflammation: Can IL‐37 play a role?

Ferulic acid increases pain threshold and ameliorates depression-like behaviors in reserpine-treated mice: behavioral and neurobiological analyses

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