Chang J Y, Korolev V V, Wang J Z
Department of Anatomy, University of Arkansas for Medical Sciences, Little Rock 72205, USA.
Neurosci Lett. 1996 Mar 15;206(2-3):181-4. doi: 10.1016/s0304-3940(96)12468-x.
Cultured cerebellar granule cells undergo programmed cell death when they are deprived of depolarizing KCl. Results from this study indicate that the cAMP analog cyclic 8-(4-chlorophenylthio) adenosine-3'5'-monophosphate (CPT-cAMP) can prevent the cell death in a dose-dependent manner, with the maximal effect seen at 500 microM. Approximately 70% of cells can be saved with this concentration of CPT-cAMP for at least 6 days. Pituitary adenylate cyclase-activating polypeptide (PACAP) increased the intracellular cAMP levels of these cells in a time- and dose-dependent manner. This agent can prevent the decrease of cAMP and cell death induced by KCl withdrawal. These results suggest that PACAP could function as a neurotrophic factor for cerebellar granule cells in vivo.
培养的小脑颗粒细胞在被剥夺去极化氯化钾时会经历程序性细胞死亡。本研究结果表明，环磷酸腺苷类似物环8-（4-氯苯硫基）腺苷-3',5'-单磷酸（CPT-cAMP）能以剂量依赖的方式预防细胞死亡，在500微摩尔时效果最佳。用该浓度的CPT-cAMP可挽救约70%的细胞至少6天。垂体腺苷酸环化酶激活多肽（PACAP）能以时间和剂量依赖的方式提高这些细胞的细胞内环磷酸腺苷水平。该药物可预防因氯化钾撤除引起的环磷酸腺苷减少和细胞死亡。这些结果表明，PACAP在体内可能作为小脑颗粒细胞的神经营养因子发挥作用。
