The stress hormone can sometimes be beneficial: this is how it activates the cells that repair the brain

The pathways of the nervous system are truly endless. And they lead to the discovery of protective mechanisms for neurons and brain connections that come into play thanks to what is considered a formidable enemy of nerve cell wellbeing: stress. In reality, stress is a genuine warning signal that prompts certain areas of the brain – primarily the hypothalamus – to release hormones that help combat the harmful effects caused by illness or trauma. In fact, stress itself may provide a sort of ‘jolt’ capable of helping the brain to repair itself following an injury, thanks to the action of a small population of cells.

These are OPCs, or oligodendrocyte progenitor cells. Research carried out on laboratory mice shows that these invisible progenitor cells, which form myelin (essentially the insulating layer that enables nerve signals to pass through correctly and which is impaired, for example, in multiple sclerosis), which is essential for the well-being of the nervous system, are in fact capable of releasing corticotropin-releasing hormone (CRH) following brain trauma; this hormone regulates the body’s stress response. Thanks to this targeted action in the area of damaged tissue, cell maturation is improved, the reconstruction of the myelin sheath is promoted, and, to some extent, the repair of the nervous system is also aided.

The research demonstrating this, published in Cell Reports, was coordinated by Jan M. Deussing of the Max Planck Institute of Psychiatry (first name Clemens Ries) and paves the way for new prospects – which are still a long way off, but which could lead to treatments for conditions such as multiple sclerosis and polyneuropathies.

In animals, in the laboratory, the activation of a particular type of cell is always observed following brain damage. In mice, Clemens Ries, as revealed in a note from the German Institute, has identified the marker for oligodendrocyte progenitor cells (OPCs). These cells are capable of maturing into oligodendrocytes, which produce the myelin sheath that covers the axons – invisible filaments that enable neurons to communicate with one another. Myelin facilitates the efficient transmission of information along axons and helps to supply them with the necessary nutrients, thus proving vital for nerve signal transmission and healthy brain function. In the event of myelin damage, the protective sheath breaks down. The restoration of myelin around damaged axons is therefore essential and represents an important part of the brain’s response to trauma.

As well as confirming this function of OPCs, the research shows that almost one in three of these progenitor cells in the area of injury produce corticotropin-releasing hormone (CRH), which plays a central role in regulating the body’s stress response. Hormone production can be detected within a few hours of the injury, but ceases after about three days. This brief and rapid activity suggests that CRH plays an important role during the very earliest stages of the healing process. But that is not all. The findings indicate that CRH helps regulate the maturation timeline of OPCs, which are therefore not only important following an injury. They also play a fundamental role in myelination during brain maturation. Much of this myelination takes place after birth and continues into early adulthood. Therefore, the potential ‘beneficial’ role of this stress-related hormone could also be crucial in the development of the nervous system and in processes of plasticity. The reparative effect is presumably mediated not only by CRH secreted by the OPC precursors themselves (OPCs) but also by developing neurons and other cells capable of producing it, thereby amplifying its action through an increased capacity to proliferate and mature into myelin-producing oligodendrocytes.