Beinfeld M C
Department of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, MA 02111, USA.
Regul Pept. 1996 Dec 3;67(2):75-7. 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 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.
细胞内cAMP升高的试剂可增强体外培养的大鼠脑片胆囊收缩素（CCK）的释放。用可增加细胞内cAMP的试剂处理培养的几种表达CCK的肿瘤细胞，可增加CCK的分泌。还研究了cAMP升高是否也会改变体外培养的大鼠脑片中钾诱导的CCK释放。用5 microM福斯可林加0.5 mM异丁基甲基黄嘌呤（3 - 异丁基 - 1 - 甲基黄嘌呤，一种磷酸二酯酶抑制剂）处理大鼠前额叶皮层和尾状核 - 壳核切片，可使钾诱导的CCK释放显著升高。cAMP可增加完整脑片以及甲状腺、胰腺、垂体和肠道内分泌肿瘤细胞中的CCK释放，这表明cAMP是调节CCK释放的常见细胞内介质。
