Zhou Y, Huang M, Shan H, Han X, Xu R
Institute of Basic Medical Sciences, CAMS, Beijing.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1995 Dec;17(6):412-7.
The effect of cholecystokinin octapeptide (CCK-8) on the release of prolactin (PRL) in male rats were studied in vivo and in vitro. CCK-8 at the concentrations (microgram) of 0.05 and 0.5 was injected into the third cerebral ventricle (3rd, V. I) of conscious rats, outfitted with chronic 3rd. V. and jugular cannulae, a significant increase in resting secretion and restraint stress-induced release of PRL were observed. The effects of CCK-8 at the concentration of 0.05 microgram were stronger than those of 0.5 microgram. To determine if CCK-8 would exert any direct action on anterior pituitary, CCK-8 of 0.05, 0.5, 1.00 microgram were added to the medium of dispersed anterior pituitary cell, and caused dose-dependent increase of PRL secretion. To study a mechanism of intracellular signal transduction in the action of CCK-8, the levels of cAMP and [Ca2+] in the medium were measured. Intracellular Ca2+ concentration of disperse anterior pituitary cell was significantly elevated by CCK-8 (2 x 10(-4) mol/L), but CCK-8 (10(-8)-10(-6) mol/L) did not change intracellular cAMP content. The results indicate that CCK-8 stimulate prolactin release at both sites of hypothalamic and anterior pituitary and the mechanism of stimulating effects of CCK-8 might be mediated by [Ca2+] but not cAMP.
在体内和体外研究了八肽胆囊收缩素(CCK-8)对雄性大鼠催乳素(PRL)释放的影响。将浓度为0.05微克和0.5微克的CCK-8注入装有慢性第三脑室和颈静脉插管的清醒大鼠的第三脑室(第三脑室,VI),观察到静息分泌和束缚应激诱导的PRL释放显著增加。0.05微克浓度的CCK-8的作用比0.5微克的更强。为了确定CCK-8是否会对垂体前叶产生任何直接作用,将0.05、0.5、1.00微克的CCK-8添加到分散的垂体前叶细胞培养基中,导致PRL分泌呈剂量依赖性增加。为了研究CCK-8作用中的细胞内信号转导机制,测量了培养基中cAMP和[Ca2+]的水平。CCK-8(2×10(-4)mol/L)使分散的垂体前叶细胞内Ca2+浓度显著升高,但CCK-8(10(-8)-10(-6)mol/L)未改变细胞内cAMP含量。结果表明,CCK-8在下丘脑和垂体前叶两个部位均刺激催乳素释放,CCK-8刺激作用的机制可能由[Ca2+]介导而非cAMP。