Abstract
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.
Highlights
The human brain is able to undergo dramatic plasticity throughout life in response to both internal and external signals
Administration of exogenous prolactin to virgin mice increases oligodendrocyte precursor cells (OPCs) proliferation [155]. This suggests that prolactin can act either directly or indirectly on OPCs to promote proliferation, these findings are in contrast to work performed in OPC-enriched neurosphere cultures derived from the adult rat hippocampus, in which seven days of prolactin treatment had no effect on cell numbers and no effect on differentiation into myelin basic protein (MBP)+ OLs [159]
Hydrocortisone treatment of primary cell cultures derived from newborn rat cortices increased transcripts and protein for three myelin markers: glycerol phosphate dehydrogenase (GPDH), a general marker of OLs, as well as MBP and proteolipid protein (PLP), proteins associated with mature
Summary
The human brain is able to undergo dramatic plasticity throughout life in response to both internal and external signals. OLs are originally derived from multipotent neural stem cells (NSCs) that maintain the capacity for selfrenewal and can differentiate to adopt a neuronal or glial fate These processes are tightly regulated by numerous factors, and the progression from NSC to mature OL can be tracked by the expression of characteristic cellular markers (Figure 1). While the downstream actions of these receptors are considerably heterogeneous, activation of many of these receptors, especially cell surface receptors, converge upon common signaling pathways, in particular the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3kinase (PI3K)/protein kinase B (AKT) signaling pathways These pathways are broadly known to regulate cellular growth and survival [38,39], and substantial gaps remain in our understanding of these hormones’ effects across the OL lineage, each of these hormones has been shown to enhance OPC proliferation and/or OL survival
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