Dynorphin A, kappa opioid receptors and the antinociceptive efficacy of asimadoline in streptozotocin-induced diabetic rats

@article{Jolivalt2006DynorphinAK,
  title={Dynorphin A, kappa opioid receptors and the antinociceptive efficacy of asimadoline in streptozotocin-induced diabetic rats},
  author={Corinne G. Jolivalt and Y. Jiang and Jason D. Freshwater and Gerd D. Bartoszyk and N. A. Calcutt},
  journal={Diabetologia},
  year={2006},
  volume={49},
  pages={2775-2785}
}
Aims/hypothesisWe investigated spinal and peripheral kappa opioid systems in diabetic rats.Materials and methodsDynorphin A, N-methyl-d-aspartate (NMDA) and kappa opioid receptor (KOR) were measured in spinal cord, dorsal root ganglia, peripheral nerves and foot skin of control and streptozotocin-induced diabetic rats by immunoassay and Western blotting. Behavioural assessments of paw tactile sensitivity and formalin-evoked hyperalgesia were performed in normal and diabetic rats before and… 
The role of κ-opioid receptor activation in mediating antinociception and addiction
TLDR
The role of KOR activation in mediating antinociception and addiction is reviewed and the possible therapeutic application of κ-agonists in the treatment of pain and drug addiction is discussed.
C-Peptide Reverses Nociceptive Neuropathy in Type 1 Diabetes
TLDR
It is concluded that C- peptide exerts beneficial therapeutic effects on diabetic nociceptive neuropathy and that optimal effects require maintenance of physiological C-peptide concentrations for a major proportion of the day.
Analgesic Effects of Duloxetine on Formalin-Induced Hyperalgesia and Its Underlying Mechanisms in the CeA
TLDR
The activation of CeA neurons may account for the transition from acute pain to long-term hyperalgesia after formalin injection, and DUL may produce potent analgesic effects on the hyperAlgesia and decrease the expressions of p-ERK through increasing the concentration of serotonin in the CeA.
Novel κ-opioid receptor agonist MB-1C-OH produces potent analgesia with less depression and sedation
TLDR
MB-1C-OH is a novel κ-opioid receptor agonist that produces potent antinociception causing less sedation and depression.
Effects of Orchidectomy and Testosterone Replacement on Numbers of Kisspeptin‐, Neurokinin B‐, and Dynorphin A‐Immunoreactive Neurones in the Arcuate Nucleus of the Hypothalamus in Obese and Diabetic Rats
TLDR
It is concluded that alterations in numbers of kisspeptin‐IR and neurokinin B‐IR neurones in the ARC and their response to ORX and ORX+T may account for disruptions of metabolic and reproductive functions in diabetic but not in obese rats.
...
...

References

SHOWING 1-10 OF 56 REFERENCES
Antinociceptive Effect of Morphine, but not &mgr; Opioid Receptor Number, Is Attenuated in the Spinal Cord of Diabetic Rats
TLDR
The reduced analgesic effect of intrathecal morphine in diabetes is probably due to impairment of &mgr; opioid receptor–G protein coupling rather than reduction in &m Gr.
Elevated spinal cyclooxygenase and prostaglandin release during hyperalgesia in diabetic rats.
TLDR
Spinal delivery of selective inhibitors of cyclooxygenase-2 or antagonists of prostaglandin receptors may have therapeutic potential for treating painful diabetic neuropathy.
Neuropathic Pain Activates the Endogenous κ Opioid System in Mouse Spinal Cord and Induces Opioid Receptor Tolerance
TLDR
It is suggested that pSNL induced a sustained release of endogenous prodynorphin-derived opioid peptides that activated an anti-nociceptive KOR system in mouse spinal cord and induced GRK3-mediated opioid tolerance.
Peripheral effects of the kappa-opioid agonist EMD 61753 on pain and inflammation in rats and humans.
TLDR
Data show differentially mediated peripheral actions of EMD 61753: kappa-opioid receptor-induced analgesia and nonopioids, non-N-methyl-D-aspartic acid hyperalgesic and proinflammatory effects.
Is the reduced efficacy of morphine in diabetic rats caused by alterations of opiate receptors or of morphine pharmacokinetics?
TLDR
The data indicate that the reduced analgesic effect of morphine caused by diabetes cannot be explained by a decrease in opiate-receptor affinity or density but rather by kinetic alteration of morphine (increase of total clearance and of volume of distribution in comparison with healthy animals).
...
...