Among a host of protective functions of the neuroglial cells, are their ability to prevent or limit damage to the brain’s neurons, which are highly sensitive, during brain infections or injury. At the Charité-Universistätsmedizin, a group of scientists conducted an inquest into the mode of action of glial cells, they established that a remodeling of the membrane and external cell structure of glial cells play a critical role in curtailing the spread of brain infection and inflammation. The conclusion of the study was published in Nature Communications, which uncovers the brain’s machinery used to curtail damages it may suffer in an aftermath of a disease or injury.
Knowing the glial cells
As we already know, neurons lack the ability to regenerate after damage. This particularly makes them prone to long-lasting injuries. If harm is done to the brain, many cells harmonize and work synergistically to elide to the effects of the harm, and also to ensure revitalization.
The brain houses several types of glial cells, astrocytes being the commonest found within the central nervous system. These astrocytes are of extreme value in sub-serving neuroprotective functions. Through the “reactive astrogliosis”, a special defense mechanism, they are able to grease the pathway of the formation of scar, which is the body’s way of downgrading inflammation and truncating the damages. In this way, astrocytes ensure the safety of the immediate nerve cells close to the site of damage, thereby maintaining the integrity and the neuronal functions.
The Berlin study
In this study, the scientists were able to explain more in the coordination of new approaches within the astrocytes, that enables them to optimize their protective functions. According to Prof. Dr. Britta Eickholt, the team leader and the Director of Charité’s Institute of Biochemistry and Molecular Biology “We were able to show for the first time that the protein ‘drebrin’ controls astrogliosis, astrocytes need drebrin to form scars and protect the surrounding tissue.” After inhibiting the synthesis of drebrin within the astrocytes of animal models, the scientists fully monitored its functions during brain injuries. Using high-resolution light microscopes and an electron microscope, they examined alterations in the brain at the cellular level, as well as culturing and constantly exploring individual astrocytes. The team leader hypothesized that “Loss of drebrin results in the suppression of normal astrocyte activation, and instead of engaging in defensive reactions, these astrocytes suffer complete loss of function and abandon their cellular identity.” If scar formation is inadequate, a little damage will disseminate, harming or even killing many standby nerve cells.
In the facilitation of a formation of scar, Drebrin regulates the remodeling of actin, an inner cytoskeleton framework that sustains the mechanical strength of the astrocytes. In that way, Drebrin can promote the production of a tubular endosome, a cylindrical structure found in the membrane, that enables assimilation, grouping, and apportioning of membrane receptors that help the astrocyte in its defensive work.
The study concluded that astrocytes play a very vital role in curtailing brain inflammation by scar formation. The functioning of these astrocytes was shown also to be greatly dependent on Drebrin which takes advantage of the fluid and adaptable cytoskeleton and cell membrane of the astrocytes to affect their neuroprotective functions.