In cases of demyelinating diseases or injury to the spinal cord, researchers observe the axonal outer, protective covering, otherwise known as myelin, becomes damaged. This damage slows down the conduction of action potentials and greatly impairs important synaptic connections. As a result of this impaired conduction, there is a lack of sensation and cognition. As a result of demyelination, serious neurological disorders arise. Many researchers have experimented with the manipulation of myelin in hopes of finding new ways to prevent its possible deterioration.
One of those researchers, Dr. Ye., along with his research team, took on the task of investigating the process behind demyelination of the axons. Specifically focused on the effects of spinal cord injury (SPI), they were interested in the functional signification of myelin and the effects of it’s deterioration on the shiverer mouse. The research team then did several experiments to test the effects of transplanting oligodendrocytes, cells that provide support and insulate the axons, into the region of the spinal cord injury. They found that after spinal cord injury, both necrosis and apoptosis are important in oligodendrocyte injury (Ye, et all.). This event causes demyelination of axons and also causes the ion channels to be exposed. They found that oligodendrocytes could be transplanted into a region of the spinal cord injury. This would then promote demyelination and eventually restoration of axonal conduction (Ye, et all). They even believe that this could be a form of rehabilitation therapy for individuals suffering from paralysis as a result of SPI. In the actual experiment, Ye and his research team began with damaging a section of the spinal cord in the shiverer mice (Ye, et all.). Upon damage, Ye’s research team observed the demyelination of the axon. Then they injected various amounts of oligodendrocytes to the damaged area of the spinal cord. The team was pleased to find that the oligodendrocytes restored myelination of part of the injured spinal cord and also organized the ion channels. Upon restoration of the myelin, they saw faster axonal conduction, enhanced high frequency signals, and a positive result to their experimentation (Ye, et all.). Overall, the team was impressed with their findings, although they believe there is still more experimentation required to completely understand the neural processes involved.
Much like Dr. Ye and his research team, other researchers are working with the effects of myelin in the brain as well as the effects that other outside factors can have on myelin. Scientists like Dr. Karen Dietz and Dr. Jia Liu, along with their research team, worked together to study the effects of how social isolation disrupts myelin production. A November article from this year titled, “New Form of Brain Plasticity: How Social Isolation Disrupts Myelin Production,” explains the work done by these two brilliant scientists. Dr. Karen Dietz is from the Department of Pharmacology and Toxicology at the UB School of Medicine and Biomedical Sciences and has done extensive work in this area. Dr. Jia Liu is from the Mt. Sinai School of Medicine. Working together, they researched the confounding factors of brain plasticity, or the brain’s ability to adjust to environmental changes. Research found that neurons are not the only structures in the brain that undergo changes in response to environmental changes.
Dr. Dietz and Dr. Lui found that changes in myelin are found in young animals or adolescents responding to environmental changes. Also they found a correlation between depression and changes in myelin. They found myelin changes in both child and adult psychiatric disorders as well. All of this shows that plasticity in the brain is not strictly limited to neurons. The research team also explains that the stresses of social isolation causes disruption in the production of oligodendrocytes (Dietz-Lui, 2012). They analyzed the brain tissue of animals that had been experimentally isolated and found these animals possessed lower levels of the gene transcription needed for oligodendrocytes. This was the first experiment that showed that environmental factors like social isolation results in a change in the production of oligodendrocytes. This is comparable to the outside factor of a spinal cord injury causing damage to the myelin levels in the brain in Dr. Ye’s experiment. Both experiments show outside factors causing levels of myelin and oligodendrocytes to change in the brain as well as how the cells/neurons in the brain will react to these changes. Dr. Dietz and Dr. Lui found that DNA compaction is what allows the oligodendrocytes to mature and produce the required amounts of myelin. They found in the animals that were socially isolated, this process of DNA compaction was not as successful, there was less compaction and therefore the oligodendrocytes were not matured (Dietz-Lui 2012). This meant less myelin was being produced.
Therefore, social isolation causes changes in the brain’s white matter, effects the oligodendrocyte’s maturity, and the production of myelin. On the other hand, they found that social interaction did just the opposite and increased the production of myelin (Dietz-Lui 2012). Both, Dr. Dietz and Dr. Lui believe this newfound information will help them learn more about the brain’s plasticity as well as the effect it has on myelin. They also believe that for patients with Multiple Sclerosis or other demyelination diseases increasing social interaction coupled with treatments might help enhance the recovery (Dietz-Lui 2012). The findings that both research teams have arrived at are important additions to our understanding of how myelin works in the brain, and just how easily damaged it can be.
Sources:
1. University at Buffalo. "New form of brain plasticity: How social isolation disrupts myelin production." ScienceDaily, 11 Nov. 2012. Web. 10 Dec. 2012.
2. Ye, Huie, Josef Buttigieg, Yudi Wan, Jian Wang, and Sarah Figley. "Expression and functional role of BK channels in chronically injured spinal cord white matter." Neurobiology of Disease 47 (2012): 225-36. Print.
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