鸟苷通过cAMP依赖性和非依赖性机制增强PC12细胞中的神经突生长。
Neurite outgrowth in PC12 cells is enhanced by guanosine through both cAMP-dependent and -independent mechanisms.
作者信息
Gysbers J W, Rathbone M P
机构信息
Department of Biomedical Sciences, Health Sciences Centre, McMaster University, Hamilton, Ontario, Canada.
出版信息
Neurosci Lett. 1996 Dec 20;220(3):175-8. doi: 10.1016/s0304-3940(96)13253-5.
Extracellular guanosine, guanosine triphosphate (GTP), and 5'-N'-ethylcarboxamidoadenosine (NECA), each significantly enhanced the proportion of nerve growth factor (NGF)-treated rat pheochromocytoma (PC12) cells which had neurites, greater than that in cultures exposed to NGF alone. Guanosine and NECA, but not GTP, increased intracellular cAMP concentrations. An adenylate cyclase inhibitor, SQ22536, completely blocked the cAMP increase induced by both guanosine and 0.1 microM NECA. However, SQ22536 only partially blocked guanosine enhanced neurite outgrowth, although it completely blocked the neuritogenic effect of NECA. Therefore guanosine-enhanced neurite outgrowth through both cAMP-dependent and -independent mechanisms, while the effect of GTP was cAMP-independent.
细胞外鸟苷、三磷酸鸟苷（GTP）和5'-N'-乙基羧酰胺腺苷（NECA）均显著提高了经神经生长因子（NGF）处理的大鼠嗜铬细胞瘤（PC12）细胞中具有神经突的细胞比例，且高于仅暴露于NGF的培养物中的比例。鸟苷和NECA可增加细胞内cAMP浓度，但GTP无此作用。腺苷酸环化酶抑制剂SQ22536完全阻断了鸟苷和0.1 microM NECA诱导的cAMP增加。然而，SQ22536仅部分阻断了鸟苷增强的神经突生长，尽管它完全阻断了NECA的促神经突形成作用。因此，鸟苷通过cAMP依赖性和非依赖性机制增强神经突生长，而GTP的作用是cAMP非依赖性的。
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