Inouye H, Kirschner D A
Department of Neuroscience, Children's Hospital, Boston, Massachusetts 02115.
Biophys J. 1988 Feb;53(2):247-60. doi: 10.1016/S0006-3495(88)83086-8.
In our accompanying paper (Inouye and Kirschner, 1988) we calculated the surface charge density at the extracellular surfaces in peripheral and central nervous system (PNS; CNS) myelins from observations on the dependency of the width of the extracellular space on pH and ionic strength. Here, we have determined the surface charge density of the membrane surfaces in myelin from its chemical composition and the localization of some of its molecular components. We then analyzed the attractive and repulsive forces between the apposed surfaces and calculated equilibrium periods for comparison with the measured values. The biochemical model accounts for the observed isoelectric range of the myelin period and, with the surface charge reduced (possibly by divalent cation binding or a space charge approximation), the model also accounts for the dependency of period on pH above the isoelectric range. At the extracellular (and cytoplasmic) surfaces the contribution of lipid (with pI approximately 2) to the net surface charge is about the same in both PNS and CNS myelin, whereas the contribution of protein depends on which ones are exposed at the two surfaces. The protein conformation and localization modulate the surface charge of the lipid, resulting in positively-charged cytoplasmic surfaces (pI approximately 9) and negatively-charged extracellular surfaces (pI approximately 2-4). The net negative charge at the extracellular surface is due in CNS myelin to lipid, and in PNS myelin to both lipid and (PO) glycoprotein. The net positive charge at the cytoplasmic surface is due in CNS myelin mostly to basic protein, and in PNS myelin to PO glycoprotein and basic protein. The invariance of the cytoplasmic packing may be due to specific short-range interactions. Our models demonstrate how the particular myelin proteins and their localization and conformation can account for the differences in inter-membrane interactions in CNS and PNS myelins.
在我们的附随论文中（Inouye和Kirschner，1988年），我们通过观察细胞外间隙宽度对pH值和离子强度的依赖性，计算了外周和中枢神经系统（PNS；CNS）髓鞘细胞外表面的表面电荷密度。在此，我们根据髓鞘的化学成分及其一些分子成分的定位，确定了髓鞘膜表面的表面电荷密度。然后，我们分析了相对表面之间的吸引力和排斥力，并计算了平衡周期，以便与测量值进行比较。该生化模型解释了观察到的髓鞘周期的等电范围，并且在表面电荷减少（可能通过二价阳离子结合或空间电荷近似）的情况下，该模型还解释了等电范围以上周期对pH值的依赖性。在细胞外（和细胞质）表面，脂质（pI约为2）对净表面电荷的贡献在PNS和CNS髓鞘中大致相同，而蛋白质的贡献则取决于哪些蛋白质暴露在两个表面。蛋白质的构象和定位调节脂质的表面电荷，导致细胞质表面带正电（pI约为9），细胞外表面带负电（pI约为2 - 4）。在CNS髓鞘中，细胞外表面的净负电荷归因于脂质，而在PNS髓鞘中则归因于脂质和（PO）糖蛋白。在CNS髓鞘中，细胞质表面的净正电荷主要归因于碱性蛋白，而在PNS髓鞘中则归因于PO糖蛋白和碱性蛋白。细胞质堆积的不变性可能归因于特定的短程相互作用。我们的模型展示了特定的髓鞘蛋白及其定位和构象如何解释CNS和PNS髓鞘中膜间相互作用的差异。
