2014
DOI: 10.1371/journal.pone.0114623 View full text |Buy / Rent full text
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Abstract: We have previously reported that enhanced excitability of dorsal root ganglia (DRG) neurons contributes to the development of bone cancer pain, which severely decreases the quality of life of cancer patients. Nav1.8, a tetrodotoxin-resistant (TTX-R) sodium channel, contributes most of the sodium current underlying the action potential upstroke and accounts for most of the current in later spikes in a train. We speculate that the Nav1.8 sodium channel is a potential candidate responsible for the enhanced excita… Show more

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“…injection of Ki16198 blocked the upregulation of EDG2 and Na v 1.8 expression in rats with bone cancer, further demonstrating that the up-regulation of EDG2 and Na v 1.8 was associated with LPA. It has been reported that Na v 1.8 influences the excitability of small and medium nociceptive DRG neurons [22], and an increase in Na v 1.8 expression contributes to mechanical allodynia [26,28,30,31,50]. It is plausible that as cancer develops, LPA released by carcinoma cells and the tumor stroma increases the excitability of peripheral C-fibers, as well as the EDG2 and Na v 1.8 expression, resulting in the enhancement of Na v 1.8 currents, further increasing the excitability of DRG neurons and thus causing mechanical allodynia.…”
Section: Discussionmentioning
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“…injection of Ki16198 blocked the upregulation of EDG2 and Na v 1.8 expression in rats with bone cancer, further demonstrating that the up-regulation of EDG2 and Na v 1.8 was associated with LPA. It has been reported that Na v 1.8 influences the excitability of small and medium nociceptive DRG neurons [22], and an increase in Na v 1.8 expression contributes to mechanical allodynia [26,28,30,31,50]. It is plausible that as cancer develops, LPA released by carcinoma cells and the tumor stroma increases the excitability of peripheral C-fibers, as well as the EDG2 and Na v 1.8 expression, resulting in the enhancement of Na v 1.8 currents, further increasing the excitability of DRG neurons and thus causing mechanical allodynia.…”
Section: Discussionmentioning
“…Na v 1.8 knockdown rats show reduced pain behavior in models of neuropathic pain and inflammatory pain [26,[28][29][30]. Compelling studies have shown that this channel is involved in the development of bone cancer pain [31] and that the Na v 1.8 currents are regulated by many inflammatory factors such as prostaglandin E2, NGF, and serotonin [24,[32][33][34]. What is more, LPA increases TTX-R currents [35].…”
Section: Introductionmentioning
“…Thermal hyperalgesia of the hindpaws was tested as described in our previous studies (3,64). Rats were allowed to acclimate for a minimum of 30 min before testing.…”
Section: Behavioral Testsmentioning
“…31 Significant reorganisation of both neuronal and supporting cell populations in the dorsal root ganglion (DRG) and dorsal horn of the spinal cord occur in response to bone metastases. 32 Mirroring primary tumours, the dorsal horn changes observed in CIBP are peculiar to the condition 33 and include neuroplastic remodelling of substantia gelatinosa excitatory fibres, raised concentrations of calcitonin gene related peptide (CGRP) 34 and increased expression of Na v 1.8 sodium channels, 35 resulting in central sensitisation and alterations in sensory modulation and transmission. 36 These changes combined with the pathophysiology of bone metastases explains the differing clinical manifestations of cancer induced bone pain, although our knowledge remains incomplete.…”
Section: Cancer Induced Bone Painmentioning