(CCK) Cholecystokinin was the first of the GUT-BRAIN PEPTIDES to be discovered: it is secreted by the DUODENUM to affect PERISTALSIS and stimulate the activity of the PANCREAS during DIGESTION and is also used as one of the NEUROTRANSMITTERS in the CENTRAL NERVOUS SYSTEM. Cholecystokinin is derived from pre-pro-cholecystokinin, a large POLYPEPTIDE composed of four domains: a 20 amino acid signal PEPTIDE (at the amino [NH2] terminus; see AMINO ACIDS); a 25 amino acid ‘spacer peptide’ (cleaved off and discarded during cholecystokinin production); a 58 amino acid domain known as cholecystokinin-58 (CCK-58) , the largest form of cholecystokinin and the part typically detected in tissues; and a C terminal peptide normally discarded during the processing of pre-pro-cholecystokinin. Further processing occurs of CCK-58 to produce cholecystokinin 8 (CCK-8), the active molecule of cholecystokinin that acts as a neurotransmitter in the central nervous system. CCK-8 is found in many parts of the brain. For example, it has a high concentration in the CEREBRAL CORTEX, and is found co-existent with DOPAMINE in the MESOLIMBIC DOPAMINE SYSTEM. It is also present in the BRAINSTEM and SPINAL CORD, in a variety of sensory ganglia, and in the RETINA.
Two types of RECEPTOR have been described, CCK1 and CCK2, at which CCK-8 is the most potent LIGAND, with GASTRIN and other CCK fragments (such as CCK-4) also active at them. Both receptors are G PROTEIN coupled.
Cholecystokinin was once thought to function as a signal of SATIETY: it is released from the duodenum during digestion, and it is found in brain. It is questionable whether it does induce feelings of satiation. For example, Ettenberg & Koob (1984) showed that satiety induced by feeding and the ‘satiety’ induced by administration of CCK had very different effects on INTRACRANIAL SELF-STIMULATION, suggesting that rats did not perceive natural satiety and that induced by CCK to be the same thing.
Ettenberg A. & Koob G.F. (1984) Different effects of cholecystokinin and satiety on lateral hypothalamic self-stimulation. Physiology and Behavior 32:127–130.
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