Stress hormone can help brain regenerate after injuries, study finds
Recent research, published by the Max Planck Institute of Psychiatry, revealed that a stress-related signal may play a key role in brain recovery after trauma. The discovery points out that precursor cells that produce myelin quickly release the stress hormone CRH near damaged brain tissue.
Unraveling the brain’s repair cells
Jan Deussing, a research group leader and experienced neurobiologist, noticed a consistent response in laboratory mice suffering brain damage: a specific group of cells activated around the injured area. Even with years of observation, the exact identity of these cells remained an enigma.
This mystery became the focus of study for Clemens Ries, who joined the Max Planck Institute of Psychiatry for an internship, approaching the completion of his biology degree. He accepted the challenge of unraveling the issue.
In a mouse model, Ries systematically tested markers for all known cell types. Only one produced a positive response: the marker for oligodendrocyte progenitor cells (OPCs).
These precursor cells have the ability to mature into oligodendrocytes, which are responsible for producing the myelin sheath. Myelin surrounds axons, which are extensions of nerve cells and allow communication between neurons. It works as an electrical insulator, optimizing the transmission of information and providing nutrients, being vital for the healthy functioning of the brain.
Damage to myelin can have serious consequences, as occurs in autoimmune diseases such as multiple sclerosis (MS), where this protective layer is degraded. Physical injuries can also compromise myelin and, in severe cases, cause the death of entire neurons. Therefore, restoration of myelin around affected axons is an essential part of the brain’s response to injury.
The surprising emergence of a stress hormone after injury
Ries’ research, initially for her master’s degree, showed that these precursor cells multiply dramatically at the edges of brain lesions. Most of them mature, transforming into oligodendrocytes capable of generating new myelin. The topic proved so intriguing that it became his doctoral thesis.
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However, Ries and Deussing discovered something unprecedented: near damaged tissue, about a third of OPCs activate corticotropin-releasing hormone (CRH), a hormone crucial in regulating the body’s stress response. Until then, it was not known that OPCs could produce neuropeptides such as CRH. The findings were published in the journal “Cell Reports”.
CRH production begins remarkably quickly, detectable within hours of an injury, but stops after approximately three days. This brief and intense release suggests that CRH has an important role in the early stages of the healing process.
The influence of CRH on myelin recovery time
One of the two known receptors for CRH also appears to be central to this process. The CRH 1 receptor is present on a different population of OPCs and allows these cells to respond to released CRH.
When CRHR1 is absent, OPCs multiply more quickly after injury. However, this initial increase does not translate into more effective repair, resulting in a smaller number of mature oligodendrocytes produced and maintained.
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Evidence indicates that CRH helps regulate the maturation time of OPCs. This control is essential for the production of mature oligodendrocytes in sufficient quantity to adequately restore the damaged myelin sheath.
The same system that shapes the developing brain
OPCs are not just important after an injury. They also play a significant role in the formation of myelin during brain maturation. Much of this myelination process occurs after birth and continues into early adulthood.
Because the CRH 1 receptor is found on OPCs even in the absence of injury, Ries and Deussing began to investigate whether it also influenced myelination during normal brain development. In collaboration with other researchers, they examined myelin formation in additional mouse models using several methods.
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They found that mice lacking the CRH 1 receptor produced more OPCs during the early stages of development. These changes did not disappear with age, but rather had lasting effects on the structure of the brain.
In adult brains, researchers have identified changes in myelination, attributed to thicker myelin sheaths, especially around thin axons. The results suggest that the CRH 1 receptor on OPCs plays an important role not only in repairing myelin after injury, but also in regulating its early development.
The origin of CRH during brain development
After injury, OPCs themselves respond by producing and releasing CRH. However, brain development raises a different question: Where does the stress hormone come from when the brain matures normally?
Scientists propose that neurons may be the answer. The hypothesis is that developing neurons release CRH, which then influences both the multiplication of OPCs and their maturation into myelin-producing oligodendrocytes.
Possible connection to depression and stress
It is already known that neurons release CRH, especially under stressful conditions. Stress experienced during early childhood development is also recognized as a risk factor for psychiatric disorders.
The new results raise the possibility that the CRH system operating in OPCs could have broader implications for mental health. Jan Deussing speculates that in stress-associated psychiatric disorders such as depression, the CRH system in OPCs may play a greater role than previously known.
If future research confirms and expands this connection, understanding how CRH signaling affects OPCs, myelin formation, and brain development could eventually point to completely new therapeutic approaches.
