Shen Pei-Juan, Yuan Chong-Gang, Ma Ji, Cheng Shuang, Yao May, Turnley Ann M, Gundlach Andrew L
Howard Florey Institute of Experimental Physiology and Medicine, The University of Melbourne, Vic. 3010, Australia.
Neuropeptides. 2005 Jun;39(3):201-5. doi: 10.1016/j.npep.2004.12.021. Epub 2005 Jan 28.
Considerable recent evidence suggests that in addition to its neuromodulatory role, galanin, like several other neuropeptides, also plays an important trophic role during development and after adult neural injury. Studies in our laboratory have identified high levels of galanin and galanin receptor expression in the subventricular zone, rostral migratory stream, subgranular zone of dentate gyrus and the medial corpus callosum--which include the main sites for continuing cell proliferation in both adult and developing rat brain. Galanin expression was also strongly and transiently induced in oligodendrocyte progenitor cells (OPCs) throughout the neocortex and corpus callosum by a benign physiological stimulus, cortical spreading depression (CSD). SD-like depolarization also occurs in peri-infarction areas following cerebral ischemia and is associated with proliferation of OPCs and transiently increased galanin expression. Together, these data suggest a putative role for galanin in regulating progenitor or 'stem cell' proliferation, migration and/or differentiation. Cultured adult and embryonic stem cells or 'neurospheres' express galanin and galanin receptor mRNA and preliminary studies suggest that sub-acute galanin treatment of cultured neurospheres decreases cell proliferation/survival, possibly by effects on the rate of apoptosis via GalR2 receptors.
最近有大量证据表明,除了其神经调节作用外,甘丙肽与其他几种神经肽一样,在发育过程中和成年神经损伤后也发挥着重要的营养作用。我们实验室的研究已经确定,在脑室下区、吻侧迁移流、齿状回颗粒下区和胼胝体中部,甘丙肽和甘丙肽受体表达水平很高,这些区域是成年和发育中的大鼠大脑中持续细胞增殖的主要部位。通过良性生理刺激——皮层扩散性抑制(CSD),甘丙肽在整个新皮层和胼胝体的少突胶质前体细胞(OPC)中也被强烈且短暂地诱导表达。类似SD的去极化也发生在脑缺血后的梗死周边区域,并与OPC的增殖和甘丙肽表达的短暂增加有关。总之,这些数据表明甘丙肽在调节祖细胞或“干细胞”的增殖、迁移和/或分化中可能发挥作用。培养的成年和胚胎干细胞或“神经球”表达甘丙肽和甘丙肽受体mRNA,初步研究表明,对培养的神经球进行亚急性甘丙肽处理会降低细胞增殖/存活,这可能是通过对经由GalR2受体的凋亡率产生影响实现的。