Stress hormone helps recover from brain injury

Research has shown that when the brain is damaged, cells activate protective mechanisms, including the release of corticotropin-releasing hormone (CRH), which promotes tissue repair.

By observing laboratory mice with brain injuries, researchers noticed that a certain type of cell was always activated near the site of injury. Their nature remained unclear, and a group of scientists at the Max Planck Institute of Psychiatry undertook to study this problem.

The team sequentially tested all known cell types and found that oligodendrocyte progenitor cells (OPCs) were activated. These cells eventually develop into oligodendrocytes, which form the myelin sheath around the axons of nerve cells. Myelin plays a key role in transmitting signals and feeding neurons, and its destruction by injury or disease such as multiple sclerosis leads to serious damage. Therefore, timely restoration of myelin is critical.

In their work, the scientists showed that OPCs actively proliferate at the edges of lesions and primarily mature into myelin-forming oligodendrocytes. They also made a surprising discovery: About a third of the OPCs in the area of ​​injury begin to produce CRH, a hormone best known for its role in the stress response. It was previously thought that OPCs were not capable of producing such neuropeptides. These results were published in the journal Cell Reports.

CRH production begins within hours of injury and continues for approximately three days, indicating its involvement in the early stages of healing. CRH receptor type 1 (CRHR1), present on another OPC population, also plays an important role. If this receptor is missing, cells multiply more quickly after injury, but fewer mature oligodendrocytes are ultimately formed. This suggests that CRH is required for proper timing of OPC maturation and efficient myelin repair.

OPCs are important not only during injury, but also during the myelination process of the developing brain, which continues from birth to young adulthood. Since the CRHR1 receptor is present on the OPC without damage, the scientists tested its role in brain development. Experiments in mice have shown that in the absence of CRHR1, more OPCs are formed early on, which subsequently affects brain structure. In adult animals, changes in myelin were observed, in particular its thickening on thin axons.

Thus, the CRHR1 receptor on oligodendrocyte progenitor cells plays a key role both in brain recovery after injury and in its normal development. When damaged, OPCs themselves produce CRH, and during brain maturation, scientists speculate that this hormone is released by neurons and regulates the proliferation and maturation of OPCs into myelin-forming cells.