垂体腺苷酸环化酶激活肽诱导PC12细胞突起生长的作用

目的　研究垂体腺苷酸环化酶激活肽（ＰＡＣＡＰ） ３８与ＰＡＣＡＰ２７ 在ＰＣ１２ 细胞突起生长中的作用，并探讨介导其作用的受体和细胞内第二信使机制。方法　采用ＰＣ１２细胞分散培养法，观察接种７２ ｈ 时ＰＣ１２ 细胞突起生长阳性细胞的百分比。结果　当ＰＡＣＡＰ３８ 和ＰＡＣＡＰ２７ 的浓度为１ ×１０－ ７ ～１ ×１０－ １１ ｍｏｌ·Ｌ－１ 之间时，均能诱导ＰＣ１２细胞突起生长，其中以１×１０ －９ ｍｏｌ·Ｌ－ １ 的浓度作用最明显，量效曲线呈“钟”形。ＰＡＣＡＰ Ⅰ型受体拮抗剂ＰＡＣＡＰ６～３８和ｃＡＭＰ依赖的蛋白激酶抑制剂ＲｐｃＡＭＰＳ 能显著地抑制ＰＡＣＡＰ诱导ＰＣ１２ 细胞突起生长的作用，而蛋白激酶Ｃ 抑制剂Ｈ７ 却没有这个作用。结论　ＰＡＣＡＰ３８ 和ＰＡＣＡＰ２７均能诱导ＰＣ１２ 细胞突起生长，该作用是由ＰＡＣＡＰ Ⅰ型受体介导的，是通过细胞内ｃＡＭＰ 依赖的蛋白激酶系统实现的

The effect of pituitary adenylate cyclase activating peptide on inducing neurite outgrowth in PC 12 cells

AIM To study the effect of PACAP 38 and PACAP 27 on inducing neurite outgrowth in PC 12 cells and the mechanism of receptor and intracelluar second messenger. METHODS The percentage of PC 12 cells exhibiting neurite outgrowth was determined after dispersed PC 12 cells were seeded for 72 h. RESULTS Both PACAP 38 and PACAP 27 could induce PC 12 extending neurites between the concentration of 1×10 -7 and 1×10 -11 mol·L -1 and the effect was maximal with 1×10 -9 mol·L -1 , forming a bell shaped dose dependency curve. PACAP Ⅰ type receptor antagonist PACAP 6～38 and cAMP dependent protein kinase antagonist R pcAMPS could significantly inhibit the effect of PACAP 38 on inducing neurite outgrowth in PC 12 cells, while protein kinase C antagonist H 7 was without effect. CONCLUSION Both PACAP 38 and PACAP 27 could induce PC 12 extending neurites, which was mediated by PACAPⅠtype receptor and cAMP dependent protein kinase.