Cholecystokinin action

Newel experimental approaches to anxiety therapy include ligands interacting with the ligand-gated ion channels that are selectively activated by nicotine, C qH 4N2 (87), the well-known active ingredient of cigarettes which has anxiolytic actions (42). Cholecystokinin B receptor ligands, specifically the dipeptoid, CI-988 [130404-91 -0] 02 1142 40 (88) have demonstrated anxiolytic activity ia preclinical models (43). 

Other peptides that have been linked to the actions of ethanol are corticotropin-releasing factor, urocortin, leptin, cholecystokinin, melanocortins, and galanin (for reviews, see Cowen et al. 2004 Egli 2003 Thiele et al. 2003). 

The regulation of food intake in humans is complex. In addition to genetic and cultural influences, it involves the action of leptin, insulin, ghrelin, PYY, cholecystokinin, and amylin. Most of these molecules act by signaling to the brain. 

Substances with a neuromodulatory effect on brain neurotransmitters by direct actions of specific receptors that modify the actions of the transmitters listed include prostaglandins, adenosine, enkephalins, substance P, cholecystokinin, endorphins, endogenous benzodiazepine receptor ligands, and possibly histamine. CNS, central nervous system. NMDA, N-methyl-D-aspartate. Strych, strychnine. 

Since food has a buffering effect, antacids are taken between meals (e.g., 1 and 3 h after meals and at bedtime). Nonabsorbable antacids are preferred. Because Mg(OH)2 produces a laxative effect (cause osmotic action, p. 170, release of cholecystokinin by Mg, or both) and Al(OH)3 produces constipation (cause astringent action of AP, p. 178), these two antacids are frequently used in combination. 

Many other neurotransmitters are undoubtedly involved in reward systems (Nutt, 1996). These include cholecystokinin, glutamate, neuropeptide Y, anan-damides and others, each of which have many other actions and also act on multiple receptor subtypes. These substances not only interact with other reward neurotransmitters but also take part in a delicate balance of activity with reciprocally connected punishment systems. 

While researchers believe that the GABAergic response is responsible for the major effects of the BZs, other mechanisms of action have been proposed. The BZs increase calcium-dependent potassium, inhibit tetrodotoxin-sensitive NA channels, and antagonize cholecystokinin-induced excitation. The clinical relevance of these actions is unknown at this time (Polk, 1988 Hobbs et ah, 1996). 

So far we have discussed the effect of CCK peptides on serotonin brain concentrations. Some evidence also exist on the action of serotonin on the CCK system. Raiteri and colleagues (1993a) looked at the effects of serotonin on the release of cholecystokinin-like immunoreactivity (CCK-LI) in synaptosomes prepared from rat cerebral cortex and nucleus accumbens. In both areas, serotonin increased the calcium-dependent depolarization-evoked CCK-LI release in a dose-related fashion. This effect was antag-... 

Bradwejn J, Koszycki D, Payeur R Study of the replication of action of cholecystokinin in panic disorders. Am J Psychiatry 149 962-964, 1992c Bradwejn J, Koszycki D, Couetoux-Dutertre AC, et al L-365,260, a CCK-B receptor antagonist, blocks CCK-4 panic (oral presentation). Presented at the annual meeting of the Anxiety Disorders Association of America (NR 235), Charleston, SC, March 20, 1993... 

Dodd J, Kelly JS The actions of cholecystokinin and related peptides on pyramidal neurones of the mammalian hippocampus. Brain Res 205 337-350, 1981... 

Kaneyuki T, Morimasa T, Shohmori T Action of peripherally administered cholecystokinin on monoaminergic and GABAergic neurons in the rat brain. Acta Med Okayama 43 153-159, 1989... 

Cholecystokinin (CCK) The tetrapeptide CCK causes more panic attacks when infused into patients with panic disorder than it does in normal volunteers, which suggests increased sensitivity of the brain type of CCK receptor, known as CCK-B. Unfortunately, in early investigations CCK-B antagonists did not appear to be effective for panic disorder. Nevertheless, agents with novel pharmacological mechanisms of action are sometimes evaluated for their potential antipanic actions by testing whether they can block CCK-induced panic attacks. 

Cholecystokinin. Cholecystokinin (CCK) is also colocalized with dopaminergic neurons and has two receptor subtypes, CCK-A being predominantly outside of and CCK-B within the central nervous system. Studies of CCK agonists and antagonists to date have not given clear clues as to their potential for therapeutic actions in schizophrenia. 

Many biologically active secreted peptides are also amidated at their carboxyl terminal, and acetylated at their amino-terminal. The consequences of these modifications are (a) to reduce the susceptibility of these peptides to degradative actions of extracellular aminopeptidases and carboxypeptidases after their secretion and (b) to influence the biological activity of the peptides. Corticotropin-releasing factor, gastrin, cholecystokinin and vasopressin require the C-terminal amide for full activity [54—56]. Acetylation of the N-terminus of a-MSH is necessary for activity, whereas acetylation of /3-endorphin inhibits its opioid activity [57], The enzymes responsible for acetylation have been identified from bovine and rat intermediate lobes [57] and enzymes with a-amidation activity have been reported in preparations of pituitary secretory granules [54,55]. 

Know the action of hormones involved in the digestion and metabolism of food substances insulin, glucagon, secretin, gastrin, and cholecystokinin. Know their chemical and physiologic properties and what controls their blood levels. 

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