Cck-KO Mouse

Cck, or cholecystokinin, is a neuropeptide and gut hormone with diverse functions. It modulates digestion, glucose levels, neurotransmitters, and memory. It is involved in pathways related to feeding behavior, central respiratory control, cardiovascular tonus, vigilance states, and nociception. Cck exerts its effects through interaction with two main receptor types, CCK-1R (formerly CCK-A) and CCK-2R (formerly CCK-B), and is of great biological importance in both the central nervous system and the gastrointestinal tract [2,3].

CCK-1R activation in the substantia nigra and striatum elicits dopamine release, and CCK-2R activation in the hippocampus and nigra has neuroprotective effects via AMPK activation, expression of mitochondrial fusion modulators, and autophagy, suggesting potential in treating Alzheimer's and Parkinson's disease [1]. Cck also acts as a peripheral satiety signal, regulating food consumption and affecting gastrointestinal motility, such as inhibiting gastric emptying and colonic transit [2,4,6]. In the context of pain modulation, Cck may act as an endogenous opiate antagonist, with small doses attenuating morphine-induced analgesia [5].

In conclusion, Cck is a multifunctional peptide with key roles in digestion, neural function, and satiety. Its functions in neurodegenerative diseases like Alzheimer's and Parkinson's, as well as in pain modulation and gastrointestinal motility, have been revealed through in-vivo studies. The understanding of Cck from these model-based research efforts provides insights into potential therapeutic strategies for related disease conditions.