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Changes in spinal cholecystokinin release after peripheral axotomy.
A W Afrah1, H Gustafsson, L Olgart
1Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden.
Neuroreport
|February 24, 2001
Summary
Following sciatic nerve injury, cholecystokinin (CCK) release in the spinal cord dorsal horn does not increase, suggesting CCK is not involved in adaptive changes after deafferentiation.
Area of Science:
- Neuroscience
- Pain Research
- Neuropeptide Signaling
Background:
- Cholecystokinin (CCK) is a neuropeptide with anti-opioid effects.
- CCK gene expression may increase in sensory neurons after peripheral nerve injury.
- Previous studies showed no increased CCK release 2-4 weeks post-sciatic nerve transection.
Purpose of the Study:
- To investigate the time course of CCK release in the spinal cord dorsal horn after sciatic nerve axotomy.
- To determine if basal and stimulated CCK levels change at various time points post-injury.
Main Methods:
- In vivo microdialysis in the spinal cord dorsal horn of rats.
- Complete transection of the sciatic nerve (axotomy).
- Measurement of CCK-like immunoreactivity (CCK-LI) after potassium stimulation (100 mM).
Main Results:
- A trend towards elevated potassium-induced CCK-LI release was observed within the first week post-axotomy.
- No significant potassium-induced CCK-LI release was detected 2-3 weeks and 2 months after axotomy.
- Basal extracellular CCK-LI levels in the dorsal horn remained unaffected.
Conclusions:
- The adaptive changes in the spinal cord dorsal horn following sciatic nerve axotomy do not involve increased CCK release.
- These findings suggest CCK does not play a role in the later stages of deafferentiation injury response.