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CCK-ergic mechanisms in sensory systems.
T Hökfelt1, K Holmberg, T J Shi
1Department of Neuroscience, Retzius Laboratory, Karolinska Institutet, Stockholm, Sweden. Tomas.Hokfelt@neuro.ki.se
Summary
Cholecystokinin (CCK) systems show distinct roles in sensory pathways, with CCK1 receptors linked to feeding regulation in rats. CCK2 receptor upregulation after nerve injury suggests roles in pain and regeneration.
Area of Science:
- Neuroscience
- Gastroenterology
- Pain Research
Background:
- Cholecystokinin (CCK) systems are implicated in sensory processing at spinal and vagal levels.
- Distinct differences exist in CCK system distribution and function across species and neural pathways.
Purpose of the Study:
- To investigate the distribution and role of cholecystokinin receptors (CCK1 and CCK2) in sensory systems.
- To explore the relationship between CCK systems, feeding regulation, and nerve injury responses.
Main Methods:
- Histochemical analysis of CCK-ergic mechanisms.
- Examination of CCK1 and CCK2 receptor expression in different neuronal populations.
- Assessment of CART peptide expression in relation to CCK receptors.
Main Results:
- CCK1 receptors are abundant in rat nodose ganglion neurons expressing CART, linking gut CCK to feeding control.
- Lower CCK1 receptor mRNA and sparse CART expression observed in rat dorsal root ganglions.
- CCK2 receptors, normally absent, are upregulated post-nerve injury, suggesting roles in regeneration and pain.
- Species differences noted, with CCK1 receptors appearing important in the human/monkey dorsal horn under normal conditions.
Conclusions:
- CCK systems play differential roles in spinal and vagal sensory pathways, with species-specific variations.
- CCK1 receptor expression is associated with feeding regulation via the CART peptide in rats.
- CCK2 receptor upregulation post-injury highlights its involvement in nerve repair and pain modulation.
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