Cholecystokinin (CCK) release from rat brain slices in vitro is enhanced by agents which elevate intracellular cAMP

• Published in: Regulatory peptides 1996-12, Vol.67 (2), p.75-77
• Main Author: Beinfeld, Margery C.
• Format: Article
• Language: English
• Subjects: 1-Methyl-3-isobutylxanthine - pharmacology; Animals; Biochemistry and metabolism; Biological and medical sciences; Brain slice; cAMP; CCK release; Central nervous system; Cholecystokinin - metabolism; Colforsin - pharmacology; Cyclic AMP - metabolism; Drug Interactions; Fundamental and applied biological sciences. Psychology; Phorbol ester; Phosphodiesterase Inhibitors - pharmacology; Potassium - pharmacology; Prefrontal Cortex - drug effects; Prefrontal Cortex - metabolism; Rats; Vertebrates: nervous system and sense organs
• ISSN: 0167-0115; 1873-1686
• DOI: 10.1016/S0167-0115(96)00115-2

Cholecystokinin (CCK) release from rat brain slices in vitro is enhanced by agents which elevate intracellular cAMP. Treatment of several CCK expressing tumor cells in culture with agents which increase intracellular cAMP increased secretion of CCK. The possibility that elevation of cAMP also alters potassium-evoked release of CCK from rat brain slices incubated in vitro was also investigated. Treatment of slices of rat prefrontal cortex and caudate-putamen with 5 μM forskolin plus 0.5 mM IBMX (3-isobutyl-1-methylxanthine, a phosphodiesterase inhibitor) caused a significant elevation of potassium-evoked CCK release. That cAMP can increase CCK release in intact brains slices as well as endocrine tumor cells from thyroid, pancreas, pituitary and intestine suggests that cAMP is a common intracellular mediator for the regulation of CCK release.