Involvement of TRPV1 in Nociceptive Behavior in a Rat Model of Cancer Pain

Shinoda, Masamichi; Ogino, Akina; Ozaki, Noriyuki; Urano, Hiroko; Hironaka, Katsunori; Yasui, Motoshi; Sugiura, Yasuo

doi:10.1016/j.jpain.2008.02.007

Cited by 57 publications

(53 citation statements)

References 54 publications

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“…The same could be true for TRPV1 based on reports that capsazepine (a selective blocker of TRPV1, which is normally involved in heat nociception, but not in mechanonociception) could reverse the decrease in threshold in a DOMS model 10 and others. 43,44,56 However, TRPV1 was not upregulated in DRG, likewise, the heat response of C-nociceptors was not altered in a reserpine-induced pain model, whereas the behavioral response to heat was clearly affected, 34 suggesting that facilitation in behavior is central in origin. Voltage-gated sodium channels such as Nav1.7, Nav1.8, and Nav1.9 expressed in peripheral nerves play crucial roles in nociception and pain, 6 and the availability of these channels is thought to determine the axonal conductive properties of nociceptors.…”

Section: Peripheral Mechanisms Of Altered Nociceptionmentioning

confidence: 93%

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: 93%

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

Taguchi

Katanosaka

Yasui

et al. 2015

Pain

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“…Analgesic effects of morphine with and without simultaneous administration of diclofenac were assessed using the Von Frey test as described by Shinoda et al [10]. Briefly, the mechanical sensitivity of the plantar surface of the hind paw was assessed using Von Frey hairs [11].…”

Section: Determination Of Analgesic Effectmentioning

confidence: 99%

<i>In Vivo</i> Interaction of Morphine and Diclofenac

Kimura¹,

Muryoi²,

Shibata³

et al. 2016

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The number of studies on possible pharmacokinetic interactions between opioid analgesics and nonsteroidal anti-inflammatory drugs (NSAIDs), which are commonly used in combination for the treatment of chronic pain, is limited. In rats, the major metabolic pathway of morphine is glucuronidation to morphine-3-glucuronide (M3G) by UDP-glucuronosyltransferase. In this study, we investigated the influence of diclofenac (NSAID) on the formation of M3G in vitro using rat liver tissue homogenates. Competitive inhibition of M3G formation by diclofenac was observed with an average Ki of 19.9 μM. Because these in vitro findings suggested that a pharmacokinetic interaction occurs in vivo, we investigated whether diclofenac inhibits the glucuronidation of morphine in rats. A single dose of diclofenac increased serum concentrations of both morphine and M3G and showed a higher analgesic efficacy in the Von Frey test. Furthermore, diclofenac caused a net decrease in morphine urine concentrations, but the excretion of M3G through biliary and urinary routes was unchanged. These results demonstrated that in contrast to in vitro data a single dose of diclofenac did not alter the glucuronidation of morphine in vivo.

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“…As a control for morphine administration, another group of rats received an equivalent volume of saline (saline group). The morphine concentration used and the subsequent timing of the behavioral observations were chosen based on previously published studies (Shinoda et al, 2008). The morphine experiment was performed blindly with respect to the drug administration.…”

Section: Measurements Of Facial Grooming Behaviorsmentioning

confidence: 99%

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

Hitomi

Ono

Miyano³

et al. 2015

Journal of Neuroscience Methods

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Involvement of TRPV1 in Nociceptive Behavior in a Rat Model of Cancer Pain

Cited by 57 publications

References 54 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

<i>In Vivo</i> Interaction of Morphine and Diclofenac

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

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Involvement of TRPV1 in Nociceptive Behavior in a Rat Model of Cancer Pain

Cited by 57 publications

References 54 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

&lt;i&gt;In Vivo&lt;/i&gt; Interaction of Morphine and Diclofenac

Novel methods of applying direct chemical and mechanical stimulation to the oral mucosa for traditional behavioral pain assays in conscious rats

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Product

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<i>In Vivo</i> Interaction of Morphine and Diclofenac