Myelination in the central nervous system depends on interactions between axons and oligodendrocyte precursor cells (OPCs). Action potentials in an axon can be followed by release of biologically active substances, like glutamate, which can instruct OPCs to start myelination. Myelin Basic Protein (MBP) is an “executive molecule of myelin” required for the formation of compact myelin. As cells of the oligodendrocyte lineage (OLCs) are capable of producing MBP in pure oligodendrocyte cultures, i.e. without neurons, we investigated Ca²⁺ signaling in developing OLCs in cultures. We show that spontaneous Ca²⁺ transients (CTs) occur at very low frequency in both bipolar OPCs and mature oligodendrocytes. In contrast immature OLCs (imOLCs), cells with several thick processes, demonstrate a relatively high frequency of CTs. Moreover, CT frequency in imOLC processes is much higher as compared with the somatic CT frequency. Somatic CTs are almost completely blocked by thapsigargin, an antagonist of sarco-(endo-) plasmic reticulum Ca²⁺ ATPase, and ryanodine, a blocker of ryanodine receptors, indicating an involvement of Ca²⁺ release from the endoplasmic reticulum. Ryanodine strongly reduces CT frequency in imOLC processes. Ouabain, an antagonist of Na⁺, K⁺-ATPase (NKA), applied at low concentration increases CT frequency, while KB-R7943, a blocker of reverse mode of Na⁺, Ca²⁺ exchanger (NCX), decreases CT frequency. We suggest that local RyR-NCX-(NKA?) interaction might underlie the generation of CTs in imOLC in the absence of neurons, and this activity influences oligodendrocyte maturation.

中枢神经系统的髓鞘形成取决于轴突和少突胶质前体细胞（OPC）之间的相互作用。轴突的动作电位之后可以释放诸如谷氨酸的生物活性物质，这可以指示OPC开始髓鞘化。髓磷脂碱性蛋白（MBP）是形成致密髓磷脂所需的“髓磷脂执行分子”。由于少突胶质细胞谱系（OLC）的细胞能够在纯少突胶质细胞培养物中（即没有神经元）产生MBP，因此我们研究了培养中的OLC的Ca ²⁺信号传导。我们证明自发的Ca ²⁺双极OPC和成熟的少突胶质细胞均以非常低的频率发生瞬态（CT）。相比之下，未成熟的OLC（imOLC）具有多个厚过程，显示出相对较高的CT频率。此外，与体CT频率相比，imOLC过程中的CT频率要高得多。躯体CT几乎完全被thapsigargin（肌氨酸-（内-））质网Ca ²⁺ ATPase的拮抗剂阻断，而ryanodine是ryanodine受体的阻滞剂，表明Ca ²⁺从内质网释放。Ryanodine大大降低了imOLC过程中的CT频率。哇巴因，Na ⁺，K ⁺的拮抗剂-低浓度的-ATPase（NKA）会增加CT频率，而Na ⁺，Ca ²⁺交换剂（NCX）的反向模式阻断剂KB-R7943会降低CT频率。我们建议，在不存在神经元的情况下，局部RyR-NCX-（NKA？）相互作用可能是imOLC中CT生成的基础，并且这种活性影响少突胶质细胞的成熟。