Pregabalin Reduces Muscle and Cutaneous Hyperalgesia in Two Models of Chronic Muscle Pain in Rats

Yokoyama, Takeshi; Maeda, Yümi; Audette, Katherine M.; Sluka, Kathleen A.

doi:10.1016/j.jpain.2006.11.007

Cited by 87 publications

(90 citation statements)

References 51 publications

(51 reference statements)

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“…In line with this, no specific pathological changes specific to acidic saline injection have been detected (Sluka et al, 2001), meaning no organic disorder has been identified that can explain the widespread pain. Intramuscular acidic saline injection model rats develop long-lasting bilateral muscle hyperalgesia (Yokoyama et al, 2007) in accordance with the deep tissue hyperalgesia and existence of tender points around the body seen in fibromyalgia patients. These animals also exhibit chronic cutaneous tactile allodynia, also consistent with findings in fibromyalgia patients.…”

Section: Face Validitysupporting

confidence: 53%

“…but significantly reduces motor function outcome, as determined by the rota-rod performance test, at 30 mg/kg i.p. or more (Yokoyama et al, 2007). This result may reflect the clinically narrow margin between analgesic and dizzying doses.…”

Section: Predictive Validitymentioning

confidence: 96%

“…However, the animal does not exhibit thermal hyperalgesia, which is measured based on paw withdrawal latency in the radiant heat exposure test. The rat displays no motor impairment, as assessed by the treadmill test, nor any histopathological change specific to the acidic acid saline injection in the affected gastrocnemius muscle (Sluka et al, 2001;Yokoyama et al, 2007).…”

Section: Primary Featuresmentioning

confidence: 98%

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Animal Models of Fibromyalgia

Nagakura¹,

Ito²,

Shimizu³

2012

New Insights Into Fibromyalgia

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Section: Face Validitysupporting

confidence: 53%

Section: Predictive Validitymentioning

confidence: 96%

Section: Primary Featuresmentioning

confidence: 98%

See 1 more Smart Citation

Animal Models of Fibromyalgia

Nagakura¹,

Ito²,

Shimizu³

2012

New Insights Into Fibromyalgia

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“…In an animal model of joint inflammation, induced by injection of kaolin and/or carrageenan into the knee joint, both primary and secondary hyperalgesia to mechanical stimuli develop [14,21,28]. Secondary hyperalgesia develops at the paw to heat and mechanical stimuli [14,24], and primary hyperalgesia is present over the inflamed knee joint [21].…”

Section: Introductionmentioning

confidence: 99%

Role of ASIC3 in the primary and secondary hyperalgesia produced by joint inflammation in mice

Ikeuchi¹,

Kolker²,

Burnes³

et al. 2008

Pain

143

140

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The acid sensing ion channel 3 (ASIC3) is critical for the development of secondary hyperalgesia as measured by mechanical stimulation of the paw following muscle insult. We designed experiments to test whether ASIC3 was necessary for the development of both primary and secondary mechanical hyperalgesia that develops after joint inflammation. We used ASIC3 -/-mice and examined the primary (response to tweezers) and secondary hyperalgesia (von Frey filaments) that develops after joint inflammation comparing to ASIC3 +/+ mice. We also examined the localization of ASIC3 to the knee joint afferents innervating the joint capsule using immunohistochemical techniques before and after joint inflammation. We show that secondary mechanical hyperalgesia does not develop in ASIC3 -/-mice. However, the primary mechanical hyperalgesia of the inflamed knee joint still develops in ASIC3 -/-mice and is similar to ASIC3 +/+ mice. In knee joint synovium from ASIC3 +/+ mice without joint inflammation, ASIC3 was not localized to joint afferents that were stained with an antibodies to protein gene product (PGP) 9.5 or calcitonin gene-related peptide (CGRP). ASIC3 was found, however, in synoviocytes of the knee joint of uninflamed mice. In ASIC3 +/+ mice with joint inflammation, ASIC3 co-localized with PGP 9.5 or CGRP in joint afferents innervating the synovium. We conclude that the decreased pH that occurs after inflammation would activate ASIC3 on primary afferent fibers innervating joint, increasing the input to the spinal cord resulting in central sensitization manifested behaviorally as secondary hyperalgesia of the paw.

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“…Coinjection of neurotrophin-3 reverses the acid-induced chronic hyperalgesia (24). Also, some muscle-derived pain can be attenuated by treatment with pregabalin or with the voltagedependent potassium M-channel openers retigabine and flupirtine (25,26). Flupirtine already is in use as an analgesic for chronic muscle pain.…”

mentioning

confidence: 99%

An antinociceptive role for substance P in acid-induced chronic muscle pain

Weinan

Chen

et al. 2011

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

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Release of substance P (SP) from nociceptive nerve fibers and activation of its receptor neurokinin 1 (NK1) are important effectors in the transmission of pain signals. Nonetheless, the role of SP in muscle pain remains unknown. Here we show that a single i.m. acid injection in mice lacking SP signaling by deletion of the tachykinin precursor 1 (Tac1) gene or coadministration of NK1 receptor antagonists produces long-lasting hyperalgesia rather than the transient hyperalgesia seen in control animals. The inhibitory effect of SP was found exclusively in neurons expressing acid-sensing ion channel 3, where SP enhances M-channel-like potassium currents through the NK1 receptor in a G protein-independent but tyrosine kinase-dependent manner. Furthermore, the SP signaling could alter action potential thresholds and modulate the expression of TTX-resistant sodium currents in medium-sized muscle nociceptors. Thus, i.m. SP mediates an unconventional NK1 receptor signal pathway to inhibit acid activation in muscle nociceptors, resulting in an unexpected antinociceptive effect against chronic mechanical hyperalgesia, here induced by repeated i.m. acid injection.is an undecapeptide belonging to the tachykinin small-peptide family (1). SP is generated in primary nociceptive sensory neurons (nociceptors) and is released with noxious stimulation (2). The release from cutaneous peripheral terminals induces neurogenic inflammation and release from central terminals enhances the glutamate-dependent excitatory postsynaptic potential, thus leading to central sensitization (3-5). Although sensory neurons in muscle also contain SP, i.m. SP injection evokes a very low level of neurogenic inflammation and no pain (6, 7).Accumulating evidence has suggested that muscle pain might be closely related to acidosis and activation of proton-sensing ion channels (8-10). Lactate and ATP sensitize this acid activation (11,12). Human and animal studies have revealed that acidosis is an effective trigger of muscle pain. Thus, chronic muscle pain can be induced in rodents by repeated i.m. injection of acid (13,14), by i.m. injection of complete Freund's adjuvant (CFA), carrageenan, capsaicin, or proinflammatory cytokines (15-18), by arterial occlusion (19), and by eccentric muscle contraction (20). These stimuli might correspond to muscle pain related to acidosis, inflammatory and ischemic myalgia, or delayed-onset muscle soreness. Although these models might not reflect fully the complicated human pain conditions, and although repetitive acidosis is not known to produce chronic pain or central sensitization in humans, these rodent models are useful for probing the underlying mechanisms and analgesic modulation of chronic muscle pain. For instance, acid-sensing ion channel 3 (ASIC3) is essential for triggering acid-induced mechanical hyperalgesia in models of i.m. injection of acid, CFA, or carrageenan (13,17,(21)(22)(23). Coinjection of neurotrophin-3 reverses the acid-induced chronic hyperalgesia (24). Also, some muscle-derived pain can be attenu...

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Pregabalin Reduces Muscle and Cutaneous Hyperalgesia in Two Models of Chronic Muscle Pain in Rats

Cited by 87 publications

References 51 publications

Animal Models of Fibromyalgia

Animal Models of Fibromyalgia

Role of ASIC3 in the primary and secondary hyperalgesia produced by joint inflammation in mice

An antinociceptive role for substance P in acid-induced chronic muscle pain

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