Articles: neuropathic-pain.
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Anesthesia and analgesia · Jul 2014
Spinal Cord Stimulation Reduces Mechanical Hyperalgesia and Restores Physical Activity Levels in Animals with Noninflammatory Muscle Pain in a Frequency-Dependent Manner.
Spinal cord stimulation (SCS) is an effective treatment for neuropathic pain, but its effect on chronic muscle pain is unclear. We designed this study to test the effect of SCS in an animal model of noninflammatory muscle pain. ⋯ The current study shows that higher frequencies of SCS (60 and 100 Hz) significantly reduce mechanical hyperalgesia of the paw and muscle in an animal model of noninflammatory muscle pain, and 60 Hz SCS restores physical activity levels of animals, not 4 Hz.
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Naringenin, a flavonoid abundant in citrus fruits, such as grapefruits, has been reported to possess anti-inflammatory properties. The present study aimed to investigate the analgesic potential of naringenin in L5 spinal nerve ligation (SNL)-induced peripheral neuropathic pain and the underlying mechanisms associated with neuroinflammation. Different doses of naringenin or saline were administered intrathecally once daily for 11 consecutive days, from 3 days prior to surgery to 7 days after surgery. ⋯ Furthermore, naringenin significantly inhibited SNL-induced activation of glial cells (astrocytes and microglia). Morover, the upregulated expression of inflammatory mediators in neuropathic pain was significantly inhibited by naringenin. Our findings suggested that repeated administration of naringenin may alleviate neuropathic pain, possibly through inhibiting neuroinflammation.
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Interleukin-17 (IL-17) is involved in a wide range of inflammatory disorders and in recruitment of inflammatory cells to injury sites. A recent study of IL-17 knock-out mice revealed that IL-17 contributes to neuroinflammation and neuropathic pain after peripheral nerve injury. Surprisingly, little is known of micro-environment modulation by IL-17 in injured sites and in pathologically related neuroinflammation and chronic neuropathic pain. ⋯ In conclusion, we provided evidence that IL-17 modulates the micro-environment at the level of the peripheral injured nerve site and regulates progression of behavioral hypersensitivity in a murine chronic neuropathic pain model. The attenuated behavioral hypersensitivity in IL-17(-/-) mice could be a result of decreased inflammatory cell infiltration to the injured site, resulting in modulation of the pro- and anti-inflammatory cytokine milieu within the injured nerve. Therefore, IL-17 may be a critical component for neuropathic pain pathogenesis and a novel target for therapeutic intervention for this and other chronic pain states.
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Biochemical pharmacology · Jun 2014
A peripherally acting, selective T-type calcium channel blocker, ABT-639, effectively reduces nociceptive and neuropathic pain in rats.
Activation of T-type Ca²⁺ channels contributes to nociceptive signaling by facilitating action potential bursting and modulation of membrane potentials during periods of neuronal hyperexcitability. The role of T-type Ca²⁺ channels in chronic pain is supported by gene knockdown studies showing that decreased Ca(v)3.2 channel expression results in the loss of low voltage-activated (LVA) currents in dorsal root ganglion (DRG) neurons and attenuation of neuropathic pain in the chronic constriction injury (CCI) model. ABT-639 is a novel, peripherally acting, selective T-type Ca²⁺ channel blocker. ⋯ ABT-639 did not attenuate hyperalgesia in inflammatory pain models induced by complete Freund's adjuvant or carrageenan. At higher doses (e.g. 100-300 mg/kg) ABT-639 did not significantly alter hemodynamic or psychomotor function. The antinociceptive profile of ABT-639 provides novel insights into the role of peripheral T-type (Ca(v)3.2) channels in chronic pain states.
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Neuroscience letters · Jun 2014
Fucoidan attenuates the existing allodynia and hyperalgesia in a rat model of neuropathic pain.
Fucoidan is an active constituent found in brown seaweeds, which have potential neuroprotection. The current study aimed to investigate the effects of fucoidan on the maintenance of neuropathic pain induced by L5 spinal nerve ligation (SNL) and the underlying mechanism related to the spinal neuroimmune responses. Animals were randomized into 5 groups: sham-operation with vehicle and SNL with vehicle or fucoidan (15, 50, and 100mg/kg). ⋯ The results showed that fucoidan caused dose-dependently attenuation of mechanical allodynia and thermal hyperalgesia. Furthermore, fucoidan could markedly inhibit neuroimmune activation characterized by glial activation, production of cytokines as well as ERK activation. The analgesic effect of intrathecal fucoidan in rats receiving SNL might partly attribute to the inhibition of neuroimmune activation associated with the maintenance of neuropathic pain.