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Related Experiment Videos

Cholecystokinin/opioid interactions.

Z Wiesenfeld-Hallin1, G de Araúja Lucas, P Alster

  • 1Karolinska Institutet, Department of Medical Laboratory Sciences and Technology, Division of Clinical Neurophysiology, Huddinge University Hospital, S-141 86, Huddinge, Sweden. zsuzsanna.wiesenfeld-hallin@neurophys.hs.sll.se

Brain Research
|December 29, 1999
PubMed
Summary
This summary is machine-generated.

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Cholecystokinin (CCK) interacts with opioids in pain pathways. Nerve injury alters CCK and opioid receptor levels, but CCK may not be directly involved in spinal hyperexcitability after nerve injury.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Pain Research

Background:

  • Cholecystokinin (CCK) acts as an anti-opioid peptide, modulating pain perception.
  • Nerve injury is known to upregulate CCK and its receptors in sensory neurons.

Purpose of the Study:

  • To investigate the interaction between CCK and opioid systems in spinal nociception.
  • To examine the role of CCK in normal and pathological pain states, specifically after nerve injury and inflammation.

Main Methods:

  • In vivo microdialysis to measure extracellular CCK levels in the dorsal horn.
  • CCK2 receptor antagonist (CI-988) administration.
  • Double-colored immunofluorescence for CCK and mu-opioid receptor (MOR) co-localization.
  • Assessment of CCK and MOR immunoreactivity (LI) in dorsal horn neurons.

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Main Results:

  • CCK2 receptor antagonism did not affect spinal hyperexcitability, suggesting CCK is not released from injured primary afferents.
  • Intravenous or intrathecal morphine increased extracellular CCK in the dorsal horn in a naloxone-reversible manner.
  • Morphine released CCK after axotomy but not during inflammation; K(+)-stimulation released CCK during inflammation but not after axotomy.
  • Partial co-localization of CCK and MOR was observed in dorsal horn neurons.
  • Axotomy, but not inflammation, decreased CCK and MOR immunoreactivity; morphine further reduced these in axotomized rats.

Conclusions:

  • CCK may not be directly involved in spinal hyperexcitability following nerve injury.
  • Opioids can modulate CCK release in the spinal cord, potentially via direct influence on CCK-containing neurons.
  • Nerve injury and opioid administration induce complex changes in CCK and MOR expression and release in the spinal cord.