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CCK(2) receptor nullification attenuates lipopolysaccharide-induced sickness behavior.
Tracey J Weiland1, Nicholas J Voudouris, Stephen Kent
1School of Psychological Science, La Trobe University, Bundoora, Victoria, Australia. Tracey.Weiland@svhm.org.au
Summary
Mice lacking cholecystokinin B (CCK2) receptors showed reduced sickness behavior after LPS administration. This suggests CCK2 receptor activation plays a role in immune-brain communication and sickness responses.
Area of Science:
- Neuroscience
- Immunology
- Physiology
Background:
- Systemic infections trigger sickness behavior, including fever and reduced activity, mediated by immune-brain communication.
- The precise mechanisms by which peripheral cytokines signal the brain remain unclear, with proposed roles for neuroimmune communication via peripheral nerves.
Purpose of the Study:
- To investigate the role of cholecystokinin B (CCK2) receptors in mediating sickness behavior induced by lipopolysaccharide (LPS).
- To explore the involvement of CCK2 receptors in the neuroimmune communication pathways underlying sickness responses.
Main Methods:
- Wild-type (WT) and CCK2 receptor knockout (CCK2KO) mice were administered varying doses of LPS (lipopolysaccharide).
- Sickness behaviors, including body temperature, activity levels, body weight, and food intake, were measured and compared between genotypes.
Main Results:
- CCK2KO mice exhibited significantly attenuated sickness behaviors compared to WT controls following LPS administration.
- The protective effects in CCK2KO mice were dose-dependent, with higher LPS doses leading to greater differences between genotypes.
- These findings suggest CCK2 receptor activation is critical for initiating and maintaining LPS-induced sickness behavior.
Conclusions:
- CCK2 receptor activation is implicated in the neuroimmune signaling pathways that generate sickness behavior.
- While vagal nerve involvement cannot be ruled out, CCK2 receptors may also mediate immune-brain communication through non-vagal routes.