Ultra-low dose naloxone upregulates interleukin-10 expression and suppresses neuroinflammation in morphine-tolerant rat spinal cords

@article{Lin2010UltralowDN,
  title={Ultra-low dose naloxone upregulates interleukin-10 expression and suppresses neuroinflammation in morphine-tolerant rat spinal cords},
  author={Shinn-Long Lin and Ru-Yin Tsai and Y. -H. Tai and Chen-Hwen Cherng and Ching-Tang Wu and Chun Chang Yeh and Chih-Shung Wong},
  journal={Behavioural Brain Research},
  year={2010},
  volume={207},
  pages={30-36}
}

Figures from this paper

Investigating the effect of Ultra-low dose naloxone on spinal BDNF and KCC2 cotransporter in morphine tolerant and hyperalgesia rats

The data suggest that BDNF and KCC2 maybe candidate molecules which are involved in tolerance and OIH and ultra- low dose of naloxone along morphine might be a valuable therapeutic potential for controlling hypersensitivity following chronic morphine administration.

Ultra-low dose (+)-naloxone restores the thermal threshold of morphine tolerant rats.

Morphine Preconditioning Protects Against LPS-Induced Neuroinflammation and Memory Deficit

The results suggest that acute morphine injection, in spite of the induction of a neuroinflammatory response and amnesia per se, exerts an antineuroinflammatory role and protects from cell death and memory deficit in an inflammatory context.

Intrathecal Gabapentin Increases Interleukin-10 Expression and Inhibits Pro-Inflammatory Cytokine in a Rat Model of Neuropathic Pain

The anti-allodynic effects of gabapentin may be caused by upregulation of IL-10 expression in the spinal cord, which leads to inhibition of the expression of pro-inflammatory cytokine expression inThe spinal cords.

Ultralow Dose of Naloxone as an Adjuvant to Intrathecal Morphine Infusion Improves Perceived Quality of Sleep but Fails to Alter Persistent Pain

The addition of an ultralow dose of intratheCal naloxone to intrathecal morphine infusion in patients with severe, persistent pain improved perceived quality of sleep and pain and was not able to show any statistically significant effects of n aloxone on pain relief, level of activity, or quality of life.

Naloxone Protects against Lipopolysaccharide-Induced Neuroinflammation and Microglial Activation via Inhibiting ATP-Sensitive Potassium Channel

Naloxone prevented LPS-induced neuroinflammation and microglial activation partially through the KATP channel, and the presence of glibenclamide (Glib), an antagonist of KATp channel, ameliorated the suppressive effects of nalox one on inflammation and microGLial activation.

Chronic Morphine-Induced Changes in Signaling at the A3 Adenosine Receptor Contribute to Morphine-Induced Hyperalgesia, Tolerance, and Withdrawal

It is demonstrated that morphine-induced OIH and antinociceptive tolerance in rats is associated with a twofold increase in adenosine kinase (ADK) expression in the dorsal horn of the spinal cord, and the intriguing possibility that A3AR agonists may be useful adjunct to opioids to manage their unwanted effects is raised.

References

SHOWING 1-10 OF 48 REFERENCES

Ultra-Low-Dose Naloxone Restores the Antinociceptive Effect of Morphine and Suppresses Spinal Neuroinflammation in PTX-Treated Rats

Results show that ultra-low-dose naloxone preserves the antinociceptive effect of morphine in PTX-treated rats, and inhibited microglial activation and suppressed cytokine expression in PTx-treated rat spinal cords.

Attenuation of Morphine Tolerance, Withdrawal-Induced Hyperalgesia, and Associated Spinal Inflammatory Immune Responses by Propentofylline in Rats

The results of this study support the hypothesis that spinal glia and proinflammatory cytokines contribute to the mechanisms of morphine tolerance and associated abnormal pain sensitivity.

A Role for Proinflammatory Cytokines and Fractalkine in Analgesia, Tolerance, and Subsequent Pain Facilitation Induced by Chronic Intrathecal Morphine

Results suggest that IL-1 and fractalkine are endogenous regulators of morphine analgesia and are involved in the increases in pain sensitivity that occur after chronic opiates.

The Role of Spinal Neuroimmune Activation in Morphine Tolerance/Hyperalgesia in Neuropathic and Sham-Operated Rats

Targeting central cytokine production and glial activation may improve the effectiveness of morphine and reduce the incidence of morphine withdrawal-induced hyperalgesia and allodynia in neuropathic pain conditions.

Amitriptyline Suppresses Neuroinflammation-dependent Interleukin-10-p38 Mitogen-activated Protein Kinase-Heme Oxygenase-1 Signaling Pathway in Chronic Morphine-infused Rats

The results suggest that the antiinflammatory effect of amitriptyline on morphine tolerance, probably acting by increasing IL-10 expression, is mediated by p38 mitogen-activated protein kinase heme oxygenase-1 signal transduction cascade.

Intrathecal cyclooxygenase inhibitor administration attenuates morphine antinociceptive tolerance in rats.

Findings and previous studies suggest that COX may be involved in the development of morphine tolerance without directly enhancing its antinociceptive effect.