Being the most complex part of the human body, it may not come as a surprise to learn that our brain can receive, process, and respond to information faster than the blink of an eye, but did you know your brain can also rewire itself? This ability, called neuroplasticity, allows your brain to add and remove connections based on the input it receives throughout your lifetime. Not only is this essential for development, but it is also the reason individuals who have lost an important function such as sight or hearing tend to develop an increased sensitivity to other senses. Although this process is essential, for reasons that are not fully understood, as we age our brains’ ability to recover and adapt to a sudden change caused by trauma is diminished. Understanding the mechanisms of neuroplasticity would be an important discovery for medical experts who may be able to help reverse this decreased function to help patients better recover from brain trauma.
In the published article “Astrocytes shape the plastic response of adult cortical neurons to vision loss”, researchers conducted a variety of experiments to examine the significance of astrocytes on neuroplasticity. These astrocytes are described as being the “maintenance cells” of the brain because of their ability to help support and nourish brain cells. Based on past research astrocytes have been shown to also play a critical role in neuroplasticity. By understanding how astrocytes work to help rewire the brain, researchers hope to use this to better understand the different processes that occur in the adult brain after trauma takes place.
To test the behavior of astrocytes during trauma, researchers surgically removed the right eye of test mice. Like humans, the brain of mice will realize the lack of signals being received from the right eye. The lack of signals from the right eye will then cause the rearrangement of connections between cells over time. After a 3 or 7 week period, the brains of the test mice were surgically removed and a chemical that binds specifically to astrocytes was introduced allowing the researchers to view any changes under a microscope.
So, did the results suggest that astrocytes should continue to be a focus when examining the mechanisms of neuroplasticity? By examining astrocyte densities over a period of weeks, the results showed an increase in astrocytes in parts of the brain responsible for vision out of a single eye. This agrees with past research suggesting the importance of astrocytes during neuroplasticity. Surprisingly, the brains examined after only three weeks of trauma also showed an increase in astrocyte density, suggesting that the cells within the brain are quick to respond to the absence of stimulation.
Although the results suggested that astrocytes take part in the rewiring process, researchers questioned whether these cells were required for this process to occur. This question was investigated using the same experiment, but a chemical was injected into the mice before the eye was removed which stopped any response of astrocytes after the surgery was complete. After a 7-week period, the researchers again surgically removed the brain and examined it under a microscope. This time there were no changes in parts of the brain that were seen in the previous experiment. This suggests that the quick response of astrocytes after an absence of information is essential to the process of neuroplasticity.
Neuroplasticity is a complex and essential process that allows our brains to develop and respond to injury. Research suggests that the quick response of astrocytes after lack of stimulation play an essential role in the rearrangement of cells within the brain. Continued research on astrocytes will be an important factor in the understanding of neuroplasticity. Research on this topic could help experts better understand the processes of the brain, and may have a major impact on the increased recovery of traumatic brain injuries.
Work Cited:
Hennes, M., Lombaert, N., Wahis, J., Van den Haute, C., Holt, M. G., & Arckens, L. (2020). Astrocytes shape the plastic response of adult cortical neurons to vision loss. Glia, 68(10), 2102-2118.


