Articles: hyperalgesia.
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Archives of oral biology · Sep 2015
Synovial TRPV1 is upregulated by 17-β-estradiol and involved in allodynia of inflamed temporomandibular joints in female rats.
Women with reproductive capability are more likely to suffer from temporomandibular disorders (TMD), with orofacial pain as the most common complaint. In the past, we focused on the role of estradiol in TMD pain through the nervous system. In this study, we explored estradiol's influence on synoviocyte gene expressions involved in the allodynia of the inflamed TMJ. ⋯ Moreover, intra-TMJ injection of TRPV1 antagonist, capsazepine, significantly attenuated allodynia of the inflamed TMJ induced by intra-TMJ injection of CFA in female rats. This article presents a possible local mechanism for estradiol that may be involved in TMJ inflammation or pain in the synovial membrane through the pain-related gene TRPV1. This finding could potentially help clinicians understand the sexual dimorphism of TMD pain.
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Neuropathic pain is a chronic condition that is difficult to be treated. Current therapies available are either ineffective or non-specific thus requiring newer treatment approaches. In this study, we investigated the antiallodynic and antihyperalgesic effects of zerumbone, a bioactive sesquiterpene from Zingiber zerumbet in chronic constriction injury (CCI)-induced neuropathic pain animal model. ⋯ Zerumbone significantly alleviated tactile and cold allodynia as well as mechanical and thermal hyperalgesia. Our findings are in comparison to the positive control drugs thatused gabapentin (20 mg/kgi.p.) and morphine (1 mg/kgi.p.). Together, these results showed that the systemic administration of zerumbone produced marked antiallodynic and antihyperalgesic effects in the CCI-induced neuropathic pain in mice and may serve as a potential lead compound for further analysis.
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Occipital nerve stimulation (ONS) is a therapy that benefits one-third of medically refractory chronic migraine (CM) patients. How ONS affects sensory thresholds and whether modulation of thresholds could predict which patients respond to the therapy remains unclear. ⋯ We show that ONS improves mechanical thresholds in a rodent CM model, but not in shams. Our finding that mechanical but not thermal thresholds are altered with ONS suggests a more significant modulation of A-α/β fibers than of C fibers. Assessing the ability of ONS to reduce mechanical thresholds during a trial period could potentially be used to predict which patients respond.
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This study was aimed to investigate the mechanisms of the modulation effect of activation of spinal Mas-related gene C (MrgC) receptors on hyperalgesia induced by intraplantar (i.pl.) injection of (Tyr6)-γ2-MSH-6-12 (MSH) or complete Freund's adjuvant (CFA). Paw withdrawal latency test and immunohistochemistry were used to observe the effect of intrathecal (i.t.) administration of MSH or BAM8-22, two selective agonists of MrgC receptor, in hyperalgesia in rats. The results showed that i.t. administration of MSH inhibited acute hyperalgesic response induced by i.pl. application of MSH, while did not change thermal nociceptive threshold in naïve rats. ⋯ The i.t. injection of BAM8-22 at a dose of 30 nmol evidently reduced the number of CFA-evoked nitric oxide synthase (NOS)-positive neurons and the expression of calcitonin gene-related peptide (CGRP)-immunoreactivity positive nerve fibers at L3-L5 segments of the spinal cord. These results suggest that the activation of MrgC receptor in CFA-induced inflammation reduces inflammatory hyperalgesia through inactivation of NOS neurons and down-regulation of CGRP expressions, and generates delayed but long-lasting anti-nociception through the endogenous activation of MOR via indirect mechanisms. Agonists for MrgC receptors may, therefore, represent a new class of antihyperalgesics for treating inflammatory pain because of the highly specific expression of their targets.
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While spinal cord astrocytes play a key role in the generation of cancer pain, there have been no studies that have examined the relationship of tumor-induced astrocyte activation and aromatase expression during the development of cancer pain. Here, we examined tumor-induced mechanical hyperalgesia and cold allodynia, and changes in Glial fibrillary acid protein (GFAP) and aromatase expression in murine models of painful and non-painful bone cancer. We demonstrate that implantation of fibrosarcoma cells, but not melanoma cells, produces robust mechanical hyperalgesia and cold allodynia in tumor-bearing mice compared to saline-injected controls. ⋯ Finally, administration of an aromatase inhibitor reduced tumor-induced hyperalgesia in fibrosarcoma-bearing animals. We conclude that a painful fibrosarcoma tumor induces a significant increase in spinal astrocyte activation and aromatase expression and that the up-regulation of aromatase plays a role in the development of bone tumor-induced hyperalgesia. Since spinal aromatase is also upregulated, but to a lesser extent, in non-painful melanoma bone tumors, it may also be neuroprotective and responsive to the changing tumor environment.