Systemic administration of 5-HT2C receptor agonists attenuates muscular hyperalgesia in reserpine-induced myalgia model

Ogino, Shuichi; Nagakura, Yukinori; Tsukamoto, Mina; Watabiki, Tomonari; Ozawa, Tohru; Oe, Tomoya; Shimizu, Yoshiyuki; Ito, Hiroyuki

doi:10.1016/j.pbb.2013.04.007

Cited by 29 publications

(14 citation statements)

References 49 publications

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“…Before the beginning of the treatment with reserpine or melatonin, rats were left housed in the animal facility for at least 1 week. The RIM animal model is based on the hypothesis that dysfunction of biogenic amine-mediated control in the central nervous system (CNS) leads to a disease condition mimicking FM [ 34 , 63 , 64 ]. In fact, reserpine is an indole alkaloid that depletes catecholamine and so blocks irreversibly the vesicular monoamine transport, causing a marked reduction in the amount of dopamine, norepinephrine and serotonin in various brain regions inducing, in turn, muscle hyperalgesia and tactile allodynia which persist for one week or longer and increases immobility time, an indicator of pain and depression [ 65 ].…”

Section: Methodsmentioning

confidence: 99%

“…In fact, reserpine is an indole alkaloid that depletes catecholamine and so blocks irreversibly the vesicular monoamine transport, causing a marked reduction in the amount of dopamine, norepinephrine and serotonin in various brain regions inducing, in turn, muscle hyperalgesia and tactile allodynia which persist for one week or longer and increases immobility time, an indicator of pain and depression [ 65 ]. In the present study, reserpine was injected subcutaneously into the back of rats once a day for 3 consecutive days at a final dose of 1 mg/kg body weight; it was dissolved in 0.5% glacial acetic acid [ 63 , 64 , 66 ]. Since reserpine treatment may cause a significant decrease in food consumption, during the treatment food pellets was placed directly in the cages, so the RIM experimental animals could feed with less difficulty.…”

Section: Methodsmentioning

confidence: 99%

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Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats

Favero

Trapletti

Bonomini

et al. 2017

IJMS

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Fibromyalgia is a chronic syndrome characterized by widespread musculoskeletal pain and an extensive array of other symptoms including disordered sleep, fatigue, depression and anxiety. Important factors involved in the pathogenic process of fibromyalgia are inflammation and oxidative stress, suggesting that ant-inflammatory and/or antioxidant supplementation might be effective in the management and modulation of this syndrome. Recent evidence suggests that melatonin may be suitable for this purpose due to its well known ant-inflammatory, antioxidant and analgesic effects. Thus, in the current study, the effects of the oral supplementation of melatonin against fibromyalgia-related skeletal muscle alterations were evaluated. In detail, 90 Sprague Dawley rats were randomly treated with reserpine, to reproduce the pathogenic process of fibromyalgia and thereafter they received melatonin. The animals treated with reserpine showed moderate alterations at hind limb skeletal muscles level and had difficulty in moving, together with significant morphological and ultrastructural alterations and expression of inflammatory and oxidative stress markers in the gastrocnemius muscle. Interestingly, melatonin, dose and/or time dependently, reduced the difficulties in spontaneous motor activity and the musculoskeletal morphostructural, inflammatory, and oxidative stress alterations. This study suggests that melatonin in vivo may be an effective tool in the management of fibromyalgia-related musculoskeletal morphofunctional damage.

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Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats

Favero

Trapletti

Bonomini

et al. 2017

IJMS

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“…26,35 A striking finding in reserpinized animals was the paradoxical changes in the mechanical sensitivity of cutaneous C-fibers: there was a decreased proportion of mechanoresponsive Cnociceptors in all C-fiber populations, whereas there was an increased magnitude in the mechanical responses of the remaining mechanoresponsive C-nociceptors. Facilitated mechanical response was also observed in mechanoresponsive muscular C-fibers.…”

Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 99%

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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“…For this animal model, biogenic amines are depleted systemically by reserpine to mimic the alterations in biogenic amines observed clinically in FMS (male rats) [ 43 - 45 ]. Repeated administration of reserpine (1 mg/kg subcutaneously, once daily, for three consecutive days) causes long-lasting widespread muscle and cutaneous hyperalgesia that is sustained for at least 1 week in both male and female rats.…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

“…Reserpine-induced mechanical hyperalgesia is reduced by administration of anticonvulsants, serotonin-norepinephrine reuptake inhibitors, and dopamine agonist drugs, but not by NSAIDs. Lorcaserin, YM-348 and vabicaserin, all 5HT2C receptor agonists, also reverse the hyperalgesia induced by reserpine (male rats) [ 45 ]. The lack of NSAID-induced analgesia, and the modulation amines, matches the pharmacological profile for managing chronic pain in FMS [ 78 , 79 ].…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

Animal models of fibromyalgia

2013

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Animal models of disease states are valuable tools for developing new treatments and investigating underlying mechanisms. They should mimic the symptoms and pathology of the disease and importantly be predictive of effective treatments. Fibromyalgia is characterized by chronic widespread pain with associated co-morbid symptoms that include fatigue, depression, anxiety and sleep dysfunction. In this review, we present different animal models that mimic the signs and symptoms of fibromyalgia. These models are induced by a wide variety of methods that include repeated muscle insults, depletion of biogenic amines, and stress. All potential models produce widespread and long-lasting hyperalgesia without overt peripheral tissue damage and thus mimic the clinical presentation of fibromyalgia. We describe the methods for induction of the model, pathophysiological mechanisms for each model, and treatment profiles.

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Systemic administration of 5-HT2C receptor agonists attenuates muscular hyperalgesia in reserpine-induced myalgia model

Cited by 29 publications

References 49 publications

Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats

Oral Supplementation of Melatonin Protects against Fibromyalgia-Related Skeletal Muscle Alterations in Reserpine-Induced Myalgia Rats

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

Animal models of fibromyalgia

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