* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download The central nervous system, or CNS for short, is composed of the
Endocannabinoid system wikipedia , lookup
Single-unit recording wikipedia , lookup
Subventricular zone wikipedia , lookup
Adult neurogenesis wikipedia , lookup
Electrophysiology wikipedia , lookup
Artificial general intelligence wikipedia , lookup
Cognitive neuroscience wikipedia , lookup
Molecular neuroscience wikipedia , lookup
Metastability in the brain wikipedia , lookup
Microneurography wikipedia , lookup
Neural oscillation wikipedia , lookup
Node of Ranvier wikipedia , lookup
Synaptogenesis wikipedia , lookup
Caridoid escape reaction wikipedia , lookup
Mirror neuron wikipedia , lookup
Neural coding wikipedia , lookup
Multielectrode array wikipedia , lookup
Stimulus (physiology) wikipedia , lookup
Clinical neurochemistry wikipedia , lookup
Neural engineering wikipedia , lookup
Axon guidance wikipedia , lookup
Central pattern generator wikipedia , lookup
Nervous system network models wikipedia , lookup
Synaptic gating wikipedia , lookup
Neuropsychopharmacology wikipedia , lookup
Circumventricular organs wikipedia , lookup
Premovement neuronal activity wikipedia , lookup
Development of the nervous system wikipedia , lookup
Pre-Bötzinger complex wikipedia , lookup
Neuroanatomy wikipedia , lookup
Feature detection (nervous system) wikipedia , lookup
Optogenetics wikipedia , lookup
The central nervous system, or CNS for short, is composed of the spinal cord and brain. Humans have a CNS that is unable to recover and regenerate damaged nerve cells, also named neurons (Brosamle, et al., 2000). This is caused by chemicals called proteoglycans that are released by neurons (Cafferty, et al., 2007). Proteoglycans are proteins that have multiple sugars attached to them, making them resemble a tangled mess (Cafferty, et al., 2007; Krekoski, et al., 2001). Although they are meant to protect the cells, the proteoglycans’ complex structures make it hard for neurons to regenerate. They encase the damaged cells and restrain them from growing through the “wall” of proteoglycans, which is meant to close the damaged site and prevent further injury. Though it is helpful, it also prevents further growth past this sealed site. Another molecule, myelin, also gets tangled around the cell, blocking it off from more space to grow into (Brosamle, et al., 2000). Luckily, recent experiments have shown that regeneration is possible. By genetically altering, electrically stimulating, and exposing chemicals to cells, proteoglycan and myelin levels can be lowered. These methods may possibly promote and guide neuronal regeneration (Al-Majed, et al., 2000; Cafferty, et al., 2007; Davies, et al., 1999). New research has shown that lowering proteoglycan and myelin levels can promote regeneration. By reducing the number of proteoglycans around the cells, neurons should then be able to grow into the new available space. One way to achieve this is by genetically altering the DNA for specific enzymes, which are molecules that can break proteoglycans (Cafferty, et al., 2007; Krekoski, et al., 2001; Steinmetz, et al., 2005). DNA for this enzyme was taken from bacteria and implanted in mice. These mice successfully produced chondroitinase ABC, the enzyme that breaks proteoglycans. The sugars were taken off of the proteins, creating a less complex structure (Cafferty, et al., 2007). Because the proteoglycans broke into shorter, smaller pieces, neurons were able to grow into more areas. Reductions of proteoglycans also allowed scars in the nerves to reform and completely fill in the damaged areas (Krekoski, et al., 2001). Scar tissue forming is important to regeneration, because they are the first stages of development of fully functional cells. Further aid, like that accomplished with chemicals such as zymosan, can create even better, clearer environments for the neurons (Steinmetz, et al., 2005). In these experiments, neurons altered to breakdown proteoglycans yielded results of recovery after injury. Another way to promote regeneration is lowering myelin levels around the cells. Myelin is a chemical released by neurons to encase themselves, acting like armor against the environment. However, the “armor” of myelin seals the cell inside. By lowering the amount of myelin, neurons can grow back into the open space. Lowering myelin levels can be done by using genetically altered viral enzymes or human anti-bodies (Brosamle, et al., 2000; Tang, et al., 2007). The DNA of neurons are altered so that viral enzymes and human anti-bodies can be made and enhanced, respectively. They are able to digest myelin, leaving little restraint on regeneration. In one study, the human IN-1 antibody was used to break long chains of myelin around the neurons. Resulting fragments of myelin could not encase the damaged neurons, allowing them to grow longer (Brosamle, et al., 2000). These severed nerves were able to grow out into damaged areas and reattach to other nerves. Using genetically altered viruses that release certain enzymes that facilitate growth is also possible. These were injected around neurons, so that their enzymes could be near the nerves. The enzymes caused parts of neurons to break through and grow out of the myelin casing without any myelin covering them (Tang, et al., 2007). Without any myelin holding the neurons back, they were able to branch out and connect with other neurons. Transplanting neurons and surrounding material from another source to the injured area has also been shown to promote regeneration. Neurons from other nerves were surgically removed and placed into the damaged site. In the new environment, the neurons grew and connected to pre-existing broken ones resulting in severed nerves being reconnected (Davies, et al., 1999). The problem with this is that transplanted nerves grow and attach to any other nerve. In other words, the wrong nerves will regenerate into the wrong areas. Nerves that communicate with muscles may grow into the skin, while nerves that interact between the brain and skin may grow into muscle. Surprisingly, electrical stimulation has been shown to guide nerves during regeneration and allow them to function correctly. In this approach, nerves are continuously shocked with pulses of electricity. Any amount of stimulation caused nerves to extend and grow into the correct areas. With this treatment, sensory nerves grew toward the skin and motor nerves grew toward muscles successfully (Al-Majed, et al., 2000). All of these methods may aid large scale human CNS recovery; while on the other hand, they also have some disadvantages. By genetically altering the nerves, enzymes that break proteoglycans and myelin will continuously do so. Proteoglycans and myelin are needed by healthy neurons to protect themselves from injury. If too many are lost, the neurons will be extremely vulnerable and will not function correctly. The enzymes will have to be modified so that they can be deactivated/activated when needed. Transplanting neurons from other hosts may also lead to the rejection of these nerve cells. The body may misjudge them as foreign invaders and attack them. Even if the neurons are taken from the same host, the surgery to remove them will cause another area of the body to be damaged. Electrical stimulation may also cause further damage. If your hands are shocked by static, you feel pain (your response to damage). This creates the possibility that prolonged electrical shock may injure other neurons. Despite the setbacks, these new treatments for neuronal regeneration are a huge step for researchers. They will soon be able to “cure” people with damaged CNS’s and problems like memory loss, concussions, and paralysis. Word Count: 999 References: Al-Majed, A. A., Neumann, C. M., Brushart, T. M., & Gordon, T. (2000). Brief electrical stimulation promotes the speed and accuracy of motor axonal regeneration. Journal of Neuroscience, 20, 2602-2608. Brosamle, C., Huber, A. B., Fiedler, M., Skerra, A., & Schwab, M. E. (2000). Regeneration of lesioned corticospinal tract fibers in the adult rat induced by a recombinant, humanized IN-1 Antibody fragment. Journal of Neuroscience, 20, 8061-8068. Cafferty, W. B. J., Yang, S. H., Duffy, P. J., Li, S., & Strittmatter, S. M. (2007). Functional axonal regeneration through astrocytic scar genetically modified to digest chondroitin sulfate proteoglycans. Journal of Neuroscience, 27, 2176-2185. Davies, S. J. A., Goucher, D. R., Doller, C., & Silver, J. (1999). Robust regeneration of adult sensory axons degenerating white matter of the adult rat spinal cord. Journal of Neuroscience, 19, 5810-5822. Krekoski, C. A., Neubauer, D., Zuo, J., & Muir, D. (2001). Axonal regeneration into acellular nerve grafts is enhanced by degradation of chondroitin sulfate proteoglycan. Journal of Neuroscience, 21, 6206-6213. Steinmetz, M. P., Horn, K. P., Tom, V. J., Miller, J. H., Busch, S. A., Nair, D., Silver, D. J., & Silver, J. (2005). Chronic enhancement of the intrinsic growth capacity of sensory neurons combined with the degradation of inhibitory proteoglycans allows functional regeneration of sensory axons through the dorsal root entry zone in the mammalian spinal cord. (2005). Journal of Neuroscience, 25, 8066-8076. Tang, X. Q., Heron, P., Mashburn, C., & Smith, G. M. (2007). Targeting sensory axon regeneration in adult spinal cord. Journal of Neuroscience, 27, 6068-6078.