Cholecystokinin (CCK) release from rat brain slices in vitro is enhanced by agents which elevate intracellular cAMP.
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 microM 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.
Beinfeld
M C
MC
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA 02111, USA.
D015056:1-Methyl-3-isobutylxanthine / Q000494:pharmacology*; D000818:Animals; D002766:Cholecystokinin / Q000378:metabolism*; D005576:Colforsin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000378:metabolism*; D004347:Drug Interactions; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology; D017397:Prefrontal Cortex / Q000187:drug effects* / Q000378:metabolism*; D051381:Rats
D010726:Phosphodiesterase Inhibitors; D005576:Colforsin; D002766:Cholecystokinin; D000242:Cyclic AMP; D011188:Potassium; D015056:1-Methyl-3-isobutylxanthine