Written by Ashima Seth and Edited by Rasheed Majzoub
Most Biology texts devote a plethora of pages to neurons, the primary signaling cells of the nervous system. However, these same texts often gloss over glial cells, which act as the glue that holds the entire nervous system together. There are several types of glial cells that serve a variety of crucial functions in the nervous system. The most abundant of these are the astrocytes, which outnumber neurons fifty-to-one. Although previously thought to be simple ‘filler’ cells, astrocytes have been found to serve a variety of crucial functions such as providing structural support to growing and mature neurons, maintaining the concentration of ions in the surrounding fluid, performing repairs to injured neurons, and preventing the entry of blood-borne disease-causing microorganisms into the brain [1]. Now, a recent study published by the Salk Institute details significant experimental data that indicates that astrocytes may play a critical role in neuroplasticity.
Neuroplasticity is the ability of one’s brain to modify itself. If you think of the brain as a complex system of electrical circuitry, plasticity is the re-wiring of those circuits to help perceive and process information more efficiently. The human brain is particularly plastic in the earliest stages of development that occur shortly before birth since it is still capable of forming new neurons at this stage– an ability that declines rapidly as we grow older. However, neuroplasticity does not stop at the developmental stage and is a dynamic process that occurs throughout one’s lifespan. This is because electrical circuits in the brain can be re-wired not just by adding new neurons, but also by altering patterns of connectivity between existing ones.
Patterns of connection between our neurons are always changing in response to novel or sustained actions such as learning a new language or engaging in exercise [2]. However, some of the more momentous examples of plasticity have been in relation to physical trauma. In these cases, though functional loss of a sensory organ (such as eyes due to blindness) leads to concurrent losses of neuronal connections associated with that organ, the body compensates for this loss with an increase in connections for other sensory organs (such as an increased sensitivity to sound in ears) [3]. The question is: what enables the re-wiring of neural circuits in response to environmental cues?
According to a study by the Salk Institute, the answer may be astrocytes. We know from previous studies that astrocytes serve a crucial role in the structuring of neural circuits in the developing brain; but so far, we knew little of their role in defining the dynamic structure of the adult brain. By first breaking open astrocytes to separate their cellular components and then studying the proteins yielded, this study discovered an astrocytic protein, Chordin-like 1 (Chrdl1), that is responsible for the maturation of neural connections.
The monumental consequences of the function of Chrdl1 are better understood through additional studies in living systems. Mouse models developed with a mutation in the genes encoding for Chrdl1 have shown disabling of the said protein and higher levels of plasticity than normal [4]. While not much is known about Chrdl1 mutations in humans; primarily due to ethical concerns regarding human experimentation, discrete studies have shown that humans with Chrdl1 mutations display enhanced memory and learning curves.
Understanding the mechanism of Chrdl1 and its influence on plasticity has far-reaching consequences for the treatment of functional loss due to physical trauma or common neurodegenerative diseases such as Parkinson’s Disease. It is important to remember, however, that while some degree of neuroplasticity in the adult brain is desirable, highly elevated plasticity in humans has been shown to disrupt the eventual maturation and stabilization of neural circuits.
References:
- Reina, O. (2016, May 13). Astrocytes: What Are They and What Do They Do? [Blog Post]. Retrieved from https://www.tempobioscience.com/blog/?p=227
- Draganski, B., Gaser, C., Busch, V., Scuierer, G., Bogdahn, U., May, A. (2004). Changes in grey matter induced by training. Nature, 427: 311-312
- Nudo, R. (2013). Recovery after brain injury: mechanisms and principles. Frontiers in Human Neuroscience, 7: 887
- Blanco-Suarez, E., Liu, T., Kopelevich, A., Allen, N. (2018). Neuron, 100(5): 1116-1132