Helen Wills Neuroscience Institute, University of California, Berkeley, CA 94720, USA.
Department of Molecular and Cellular Biology, University of California, Berkeley, CA 94720, USA.
Biomolecules. 2021 Feb 14;11(2):283. doi: 10.3390/biom11020283.
The brain's capacity to respond to changing environments via hormonal signaling is critical to fine-tuned function. An emerging body of literature highlights a role for myelin plasticity as a prominent type of experience-dependent plasticity in the adult brain. Myelin plasticity is driven by oligodendrocytes (OLs) and their precursor cells (OPCs). OPC differentiation regulates the trajectory of myelin production throughout development, and importantly, OPCs maintain the ability to proliferate and generate new OLs throughout adulthood. The process of oligodendrogenesis, the creation of new OLs, can be dramatically influenced during early development and in adulthood by internal and environmental conditions such as hormones. Here, we review the current literature describing hormonal regulation of oligodendrogenesis within physiological conditions, focusing on several classes of hormones: steroid, peptide, and thyroid hormones. We discuss hormonal regulation at each stage of oligodendrogenesis and describe mechanisms of action, where known. Overall, the majority of hormones enhance oligodendrogenesis, increasing OPC differentiation and inducing maturation and myelin production in OLs. The mechanisms underlying these processes vary for each hormone but may ultimately converge upon common signaling pathways, mediated by specific receptors expressed across the OL lineage. However, not all of the mechanisms have been fully elucidated, and here, we note the remaining gaps in the literature, including the complex interactions between hormonal systems and with the immune system. In the companion manuscript in this issue, we discuss the implications of hormonal regulation of oligodendrogenesis for neurological and psychiatric disorders characterized by white matter loss. Ultimately, a better understanding of the fundamental mechanisms of hormonal regulation of oligodendrogenesis across the entire lifespan, especially in vivo, will progress both basic and translational research.
大脑通过激素信号对不断变化的环境做出反应的能力对于精细的功能至关重要。越来越多的文献强调了髓鞘可塑性作为成年大脑中一种突出的经验依赖性可塑性的作用。髓鞘可塑性由少突胶质细胞（OLs）及其前体细胞（OPCs）驱动。OPC 分化调节髓鞘生成的轨迹在整个发育过程中，重要的是，OPC 保持增殖和产生新的 OL 的能力在整个成年期。少突胶质细胞发生，即新 OL 的产生，可以在早期发育和成年期受到内部和环境条件（如激素）的极大影响。在这里，我们回顾了描述激素对生理条件下少突胶质细胞发生的调节的现有文献，重点介绍了几类激素：类固醇、肽和甲状腺激素。我们讨论了在少突胶质细胞发生的每个阶段的激素调节，并描述了已知的作用机制。总体而言，大多数激素都增强了少突胶质细胞发生，增加了 OPC 的分化，并诱导 OL 成熟和髓鞘生成。这些过程的机制因每种激素而异，但最终可能会通过 OL 谱系中表达的特定受体共同趋同于常见的信号通路。然而，并非所有的机制都已完全阐明，在这里，我们注意到文献中的剩余空白，包括激素系统与免疫系统之间的复杂相互作用。在本期的配套文章中，我们讨论了激素调节少突胶质细胞发生对以白质丢失为特征的神经和精神疾病的影响。最终，更好地理解整个生命周期（尤其是在体内）激素对少突胶质细胞发生的基本调节机制，将促进基础和转化研究的发展。
