Ghogha Atefeh, Bruun Donald A, Lein Pamela J
Department of Molecular Biosciences, University of California, Davis, CA, USA.
J Vis Exp. 2012 Mar 21(61):3546. doi: 10.3791/3546.
The shape of the dendritic arbor determines the total synaptic input a neuron can receive (1-3), and influences the types and distribution of these inputs (4-6). Altered patterns of dendritic growth and plasticity are associated with impaired neurobehavioral function in experimental models (7), and are thought to contribute to clinical symptoms observed in both neurodevelopmental disorders (8-10) and neurodegenerative diseases (11-13). Such observations underscore the functional importance of precisely regulating dendritic morphology, and suggest that identifying mechanisms that control dendritic growth will not only advance understanding of how neuronal connectivity is regulated during normal development, but may also provide insight on novel therapeutic strategies for diverse neurological diseases. Mechanistic studies of dendritic growth would be greatly facilitated by the availability of a model system that allows neurons to be experimentally switched from a state in which they do not extend dendrites to one in which they elaborate a dendritic arbor comparable to that of their in vivo counterparts. Primary cultures of sympathetic neurons dissociated from the superior cervical ganglia (SCG) of perinatal rodents provide such a model. When cultured in defined medium in the absence of serum and ganglionic glial cells, sympathetic neurons extend a single process which is axonal, and this unipolar state persists for weeks to months in culture (14,15). However, the addition of either bone morphogenetic protein-7 (BMP-7) (16,17) or Matrigel (18) to the culture medium triggers these neurons to extend multiple processes that meet the morphologic, biochemical and functional criteria for dendrites. Sympathetic neurons dissociated from the SCG of perinatal rodents and grown under defined conditions are a homogenous population of neurons (19) that respond uniformly to the dendrite-promoting activity of Matrigel, BMP-7 and other BMPs of the decapentaplegic (dpp) and 60A subfamilies (17,18,20,21). Importantly, Matrigel- and BMP-induced dendrite formation occurs in the absence of changes in cell survival or axonal growth (17,18). Here, we describe how to set up dissociated cultures of sympathetic neurons derived from the SCG of perinatal rats so that they are responsive to the selective dendrite-promoting activity of Matrigel or BMPs.
树突分支的形状决定了神经元能够接收的突触输入总量(1 - 3),并影响这些输入的类型和分布(4 - 6)。在实验模型中,树突生长和可塑性模式的改变与神经行为功能受损有关(7),并且被认为导致了在神经发育障碍(8 - 10)和神经退行性疾病(11 - 13)中观察到的临床症状。这些观察结果强调了精确调节树突形态的功能重要性,并表明确定控制树突生长的机制不仅将推动对正常发育过程中神经元连接如何被调节的理解,还可能为多种神经疾病的新型治疗策略提供见解。如果有一个模型系统,能让神经元通过实验从无树突延伸的状态转变为能形成与体内对应神经元相当的树突分支的状态,那么树突生长的机制研究将得到极大促进。从围产期啮齿动物颈上神经节(SCG)分离的交感神经元原代培养物提供了这样一个模型。当在无血清和神经节神经胶质细胞的特定培养基中培养时,交感神经元伸出一个单一的轴突样突起,并且这种单极状态在培养中持续数周甚至数月(14,15)。然而,向培养基中添加骨形态发生蛋白 - 7(BMP - 7)(16,17)或基质胶(18)会促使这些神经元伸出多个符合树突形态、生化和功能标准的突起。从围产期啮齿动物SCG分离并在特定条件下生长的交感神经元是一群同质的神经元(19),它们对基质胶、BMP - 7以及果蝇中dpp和60A亚家族的其他骨形态发生蛋白(BMP)的树突促进活性有一致的反应(17,18,20,21)。重要的是,基质胶和BMP诱导的树突形成发生时,细胞存活率和轴突生长没有变化(17,18)。在这里,我们描述如何建立从围产期大鼠SCG分离的交感神经元解离培养物,使其对基质胶或BMPs的选择性树突促进活性有反应。