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Painful Diabetic Neuropathy: Prevention or Suppression?
1School of Medicine, University of Colorado Anschutz Medical Campus, Aurora, CO, United States.
International Review of Neurobiology
|May 3, 2016
Summary
Peripheral diabetic neuropathy (PDN) causes pain due to sensitized neurons. Targeting ion channel modifications, not the channels themselves, may offer safer, effective treatments for PDN pain.
Area of Science:
- Neuroscience
- Pharmacology
- Diabetology
Background:
- Diabetic peripheral neuropathy (PDN) causes pain via sensitized nociceptors in the dorsal root ganglia (DRG) and dorsal horn (DH).
- Current PDN treatments are limited by nonspecific systemic drugs with side effects and abuse potential.
- Ion channel dysregulation in DRG and DH neurons contributes to nociceptor hyperexcitability in PDN models.
Purpose of the Study:
- To explore the role of posttranslational modifications in nociceptive ion channel activity in PDN.
- To identify potential therapeutic targets for painful PDN by understanding these regulatory mechanisms.
Main Methods:
- Investigated ion channel dysregulation in animal models of type 1 and type 2 PDN.
- Examined the effects of targeting posttranslational modifications, including glycosylation and methylglyoxal metabolism, on nociceptive ion channels in vivo.
Main Results:
- Dysregulated ion channels in DRG and DH neurons enhance nociceptor excitability in PDN.
- Targeting posttranslational modifications of nociceptive ion channels reversed hyperalgesia in diabetic animals with PDN.
Conclusions:
- Posttranslational regulation of nociceptive ion channels is a key mechanism in painful PDN.
- Pharmacological targeting of specific pathogenic mechanisms, rather than ion channels directly, may lead to safer and less abusable therapies for PDN.
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