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Related Experiment Videos

Central inhibitory dysfunctions: mechanisms and clinical implications.

Z Wiesenfeld-Hallin1, H Aldskogius, G Grant

  • 1Karolinska Institute, Department of Medical Laboratory Sciences and Technology, Huddinge, Sweden. zswh@bimd01.hs.sll.se

The Behavioral and Brain Sciences
|March 31, 1999
PubMed
Summary

Nervous system injury can cause persistent pain. This study shows that gamma-aminobutyric acid (GABA) and cholecystokinin (CCK) pathways are involved in pain development and opioid insensitivity after neural injury.

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Area of Science:

  • Neuroscience
  • Pain Research
  • Pharmacology

Background:

  • Nervous system injuries often lead to persistent pain, including mechanical allodynia.
  • Existing treatments, like opioids, can be ineffective for neuropathic pain.
  • Dysregulation of inhibitory neurotransmitters like GABA and endogenous opioids is implicated in pain.

Purpose of the Study:

  • To investigate the roles of GABA and cholecystokinin (CCK) in neuropathic pain after central and peripheral nervous system injury.
  • To explore the mechanisms underlying opioid insensitivity in chronic pain models.
  • To evaluate potential therapeutic targets for neuropathic pain.

Main Methods:

  • Induction of spinal cord ischemia and peripheral nerve injury in rats.
  • Assessment of mechanical allodynia-like behaviors.

Related Experiment Videos

  • Pharmacological manipulation using GABA-B receptor agonist (baclofen) and CCK-B receptor antagonist (CI 988).
  • Measurement of GABA, CCK, and CCK-receptor expression.

    • Main Results:

    • Spinal cord ischemia induced mechanical allodynia, responsive to baclofen in its acute phase.
    • Reduced GABA immunoreactivity was observed in the dorsal horn of allodynic rats.
    • Peripheral nerve injury led to upregulation of CCK and CCK-R in dorsal root ganglia.
    • CCK-B antagonist CI 988 reversed allodynia and autotomy in chronic pain models, suggesting CCK involvement in opioid insensitivity.
    • Morphine was ineffective in chronic pain models, but CCK-B antagonism restored sensitivity.

    Conclusions:

    • GABAergic dysfunction contributes to acute pain after spinal cord injury.
    • Upregulation of CCK and its receptors in the CNS and peripheral nervous system plays a critical role in chronic neuropathic pain and opioid insensitivity.
    • Targeting CCK pathways offers a potential strategy for managing neuropathic pain and overcoming opioid resistance.