Central glial activation mediates cancer-induced pain in a rat facial cancer model

Hidaka, K.; Ono, Kentaro; Harano, Nozomu; Sago, Teppei; Nunomaki, Masahito; Shiiba, Shunji; Nakanishi, Osamu; Fukushima, Hiroshi; Inenaga, Kiyotoshi

doi:10.1016/j.neuroscience.2011.02.007

Cited by 24 publications

(11 citation statements)

References 41 publications

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“…Similarly, glial activation was also induced in the MDH after trigeminal nerve ligation or transection [9-11,36], orofacial inflammation [11,62], and tumor cells inoculation in the vibrissal pad [63]. Consistent with these studies, we found that the astrocytes in the MDH changed their morphological features and manifested large somata with many thick processes from 3 days to 21 days after IAMNT.…”

Section: Discussionsupporting

confidence: 84%

Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain

Zhang

Dong

et al. 2012

J Neuroinflammation

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BackgroundNeuropathic pain in the trigeminal system is frequently observed in clinic, but the mechanisms involved are largely unknown. In addition, the function of immune cells and related chemicals in the mechanism of pain has been recognized, whereas few studies have addressed the potential role of chemokines in the trigeminal system in chronic pain. The present study was undertaken to test the hypothesis that chemokine C-C motif ligand 2 (CCL2)-chemokine C-C motif receptor 2 (CCR2) signaling in the trigeminal nucleus is involved in the maintenance of trigeminal neuropathic pain.MethodsThe inferior alveolar nerve and mental nerve transection (IAMNT) was used to induce trigeminal neuropathic pain. The expression of ATF3, CCL2, glial fibrillary acidic protein (GFAP), and CCR2 were detected by immunofluorescence histochemical staining and western blot. The cellular localization of CCL2 and CCR2 were examined by immunofluorescence double staining. The effect of a selective CCR2 antagonist, RS504393 on pain hypersensitivity was checked by behavioral testing.ResultsIAMNT induced persistent (>21 days) heat hyperalgesia of the orofacial region and ATF3 expression in the mandibular division of the trigeminal ganglion. Meanwhile, CCL2 expression was increased in the medullary dorsal horn (MDH) from 3 days to 21 days after IAMNT. The induced CCL2 was colocalized with astroglial marker GFAP, but not with neuronal marker NeuN or microglial marker OX-42. Astrocytes activation was also found in the MDH and it started at 3 days, peaked at 10 days and maintained at 21 days after IAMNT. In addition, CCR2 was upregulated by IAMNT in the ipsilateral medulla and lasted for more than 21 days. CCR2 was mainly colocalized with NeuN and few cells were colocalized with GFAP. Finally, intracisternal injection of CCR2 antagonist, RS504393 (1, 10 μg) significantly attenuated IAMNT-induced heat hyperalgesia.ConclusionThe data suggest that CCL2-CCR2 signaling may be involved in the maintenance of orofacial neuropathic pain via astroglial–neuronal interaction. Targeting CCL2-CCR2 signaling may be a potentially important new treatment strategy for trigeminal neuralgia.

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Section: Discussionsupporting

confidence: 84%

Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain

Zhang

Dong

et al. 2012

J Neuroinflammation

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“…Animal models have been developed for both of these etiologies. Tumor-related pain has been modeled following local xenograft of cancer cells [162] into the orofacial region to model orofacial pain [76;129] or bone to model metastasis-induced bone pain [81;82;112;117;165;203]. These models produce enhanced mechanical and thermal sensitivity, enhanced palpation-induced pain, and reduced grip force (movement-evoked pain), symptoms that are common in people with cancer pain.…”

Section: Animal Models Of Diseasementioning

confidence: 99%

An Overview of Animal Models of Pain: Disease Models and Outcome Measures

Gregory

Harris

Robinson

et al. 2013

The Journal of Pain

319

255

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Pain is ultimately a perceptual phenomenon. It is built from information gathered by specialized pain receptors in tissue, modified by spinal and supraspinal mechanisms, and integrated into a discrete sensory experience with an emotional valence in the brain. Because of this, studying intact animals allows the multidimensional nature of pain to be examined. A number of animal models have been developed, reflecting observations that pain phenotypes are mediated by distinct mechanisms. Animal models of pain are designed to mimic distinct clinical diseases to better evaluate underlying mechanisms and potential treatments. Outcome measures are designed to measure multiple parts of the pain experience including reflexive hyperalgesia measures, sensory and affective dimensions of pain and impact of pain on function and quality of life. In this review we discuss the common methods used for inducing each of the pain phenotypes related to clinical pain syndromes, as well as the main behavioral tests for assessing pain in each model.

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“…Nocifensive behaviors, including grooming-like and withdrawal behaviors, have traditionally been measured as signs of spontaneous and/or evoked nociception in the hind paw and orofacial regions, such as the whisker pad skin (Krzyzanowska and Avendano, 2012). Most facial grooming behaviors, including mouth rubbing (licking) and wiping by the forelimbs, have been used as signs of orofacial pain in models of inflammatory, neuropathic and cancer pain (Chidiac et al, 2002;Clavelou et al, 1989;Harano et al, 2010;Hidaka et al, 2011;Hitomi et al, 2012;Ono et al, 2009;Pelissier et al, 2002;Sago et al, 2012;Shimada and LaMotte, 2008). However, facial scratching by the hind paw is considered to reflect an itch sensation rather than pain (Shimada and LaMotte, 2008).…”

Section: Introductionmentioning

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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Central glial activation mediates cancer-induced pain in a rat facial cancer model

Cited by 24 publications

References 41 publications

Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain

Chemokine CCL2 and its receptor CCR2 in the medullary dorsal horn are involved in trigeminal neuropathic pain

An Overview of Animal Models of Pain: Disease Models and Outcome Measures

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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