作者: AM Pooler , DH Guez , R Benedictus , RJ Wurtman , None
DOI: 10.1016/J.NEUROSCIENCE.2005.03.050
关键词:
摘要: During rapid cell growth the availability of phospholipid precursors like cytidine triphosphate and diacylglycerol can become limiting in formation key membrane constituents phosphatidylcholine. Uridine, a normal plasma constituent, be converted to PC12 [corrected] cells intact brain, has been shown produce resulting increase phosphatidylcholine synthesis. To determine whether treatments that elevate uridine also thereby augment production, we exposed which had differentiated by nerve factor various concentrations uridine, measured numbers neurites produced. After 4 but not 2 days significantly dose-dependently increased number per cell. This was accompanied increases neurite branching levels proteins neurofilament M 70. Uridine treatment intracellular triphosphate, suggests may affect outgrowth enhancing stimulate neuritogenesis second mechanism, since mimicked exposing could blocked drugs known antagonize P2Y receptors (suramin; Reactive Blue 2; pyridoxal-phosphate-6-azophenyl-2',4' disulfonic acid). Treatment with or stimulated their accumulation inositol phosphates, this effect acid. Moreover, degradation nucleotides apyrase stimulatory on neuritogenesis. Taken together these data indicate regulate output from differentiating cells, suggest it does so two ways, i.e. both acting through as precursor for biosynthesis an agonist receptors.