Articles: hyperalgesia.
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Brachial plexus pain is thought to be generated not by avulsed roots but rather by nonavulsed roots, because avulsed roots could not transmit action potentials to central nerves. The aim of this study was to evaluate pain-related behavior and the extent of glial activation in a model of brachial plexus avulsion (BPA). ⋯ Our findings may indicate why neuropathic pain is so frequent and intense following BPA injury.
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It has been reported that Toll-like receptor 4 (TLR4), which plays an important role in glial activation in neuropathic pain, is significantly increased in cancer pain. The present study was designed to assess the role of TLR4 in cancer-induced bone pain (CIBP) by intrathecal administration of TLR4 signaling pathway blocker naloxone or lipopolysaccharide Rhodobacter sphaeroides (LPS-RS). ⋯ In contrast, the same pharmacological treatment showed no or slight pain relieving effect at day 16. Our findings demonstrate that the spinal TLR4 signaling pathway contributes to the mechanism underlying CIBP in a stage-dependent manner in rats, and it may be an efficacious target at early stage for the treatment in the future.
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Acta neurochirurgica · May 2013
L6 spinal nerve ligation produces prolonged development of mechanical allodynia and gradual increase of GFAP on ipsilateral dorsal horn.
L5/6 spinal nerve ligation (SNL), one of the most widely used approaches rat models for neuropathic pain, results in the rapid development of mechanical allodynia within 24-72 h. However, the result of a single L6 SNL remains unclear. ⋯ Single L6 SNL might be used as an effective model for researching the development period of neuropathic pain and is thus worth further investigation.
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Chem. Biol. Interact. · Apr 2013
Antagonism of the transient receptor potential ankyrin 1 (TRPA1) attenuates hyperalgesia and urinary bladder overactivity in cyclophosphamide-induced haemorrhagic cystitis.
The aim of this study was to investigate the involvement of the transient receptor potential ankyrin 1 (TRPA1) in haemorrhagic cystitis, the main side effect of cyclophosphamide-based chemotherapy. Hannover female rats received intraperitoneal (i.p.) injection of cyclophosphamide (three doses of 100 mg/kg, every other day, in a total of five days). This treatment was followed by the treatment with TRPA1 antagonist HC 030031 (50 mg/kg, p.o.). ⋯ The treatment with HC 030031 either before (100 mg/kg, p.o.) or after (30 mg/kg, i.v.) cyclophosphamide inhibited the non-voiding contractions but failed to counteract the loss in voiding efficiency. Our data demonstrates that nociceptive symptoms and urinary bladder overactivity caused by cyclophosphamide, in part, are dependent upon the activation of TRPA1. In this context, the antagonism of the receptor may be an alternative to minimise the urotoxic symptoms caused by this chemotherapeutic agent.