An Examination of the Human Brain: Evidence of Neuroplasticity and Neurogenesis
An Examination of the Human Brain: Evidence of Neuroplasticity and Neurogenesis My eyes snapped open even though I was scared of the sight in front of me. I watched my sister convulse and desperately gasp for air. Her eyes frantically darted up and down while all the blood drained from her face, turning it a pale pasty blue. That was only on the outside; inside her brain, a multitude of neurons was firing signals abnormally to cause the epileptic seizure. A life time of epilepsy would eventually lead to brain cell loss which was once thought to be irreversible; however, new research reveals that the connections and the number of neurons in the brain are not fixed. In the field of neuroscience, it was a long held belief that humans are born with their full set of neurons and that neurogenesis is impossible after birth. Recent studies disprove this deeply embedded doctrine—Ramon and Cajal’s hypothesis that neurogenesis occurs exclusively during prenatal development. An examination of hemispherectomy patients, the brain in periods of learning, and brains with Huntington’s disease reveals the extent of the brain’s plasticity. These examples will give insight and a more extensive understanding of the capacity and function of the human brain. Both of these aspects are interconnected and strongly linked to the brain’s neuroplasticity, including neurogenesis as an important mechanism. The brain’s capacity and function change as morphological changes occur in the brain because there is a causational relationship.
Specifically, this is true because neuroplasticity is a “…morphological modification in a cell or group of cells that changes intercellular communication” and neurogenesis refers to the birth of new neurons (Shaw et. al., 2001).” Moreover, intercellular communication is pertinent to the brain’s functional ability and intellectual ability—it governs cellular interaction and activity which is the basis for cell signaling. In this sense, the capacity of the brain refers to its intellectual ability: memory retention, logical reasoning, and potential to learn by making connections. Thus, the capacity and function of the brain are the direct results of its shape and malleability. ...
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Specifically, this is true because neuroplasticity is a “…morphological modification in a cell or group of cells that changes intercellular communication” and neurogenesis refers to the birth of new neurons (Shaw et. al., 2001).” Moreover, intercellular communication is pertinent to the brain’s functional ability and intellectual ability—it governs cellular interaction and activity which is the basis for cell signaling. In this sense, the capacity of the brain refers to its intellectual ability: memory retention, logical reasoning, and potential to learn by making connections. Thus, the capacity and function of the brain are the direct results of its shape and malleability. Such an example is a brain that has undergone a hemispherectomy procedure which demonstrates the brain’s ability to re-wire itself to perform other functions. The brain is a bilateral organ—separated into two hemispheres— which has functions that are specific to a particular area. In this procedure, one side of the brain is completely removed which would seemingly eliminate any use of these localized functions. However, studies have presented cases where patients have undergone a complete hemispherectomy (left hemisphere) yet retained their ability to speak (Machado 2007). Localized areas in the left hemisphere of the brain are responsible for linguistic function; thus its removal should have eliminated any ability to produce language. However, in children, the intact hemisphere compensates for the lost hemisphere by performing some of its functions. The right hemisphere reorganizes and generates new connections between unharmed neurons via mechanisms like axonal sprouting, “…described as the detection of axon terminals in areas previously free of those types of axon endings (Woolf et. al., 1992).” In response to the hemispherectomy, the unharmed neurons grow nerve endings to connect with neurons that had damaged or severed axons to form neural pathways. Such pathways and neuroplasticity allow the intact hemisphere to take over other functions. In this case, neuroplasticity plays a healing role to compensate for injury to the brain; furthermore, neuroplasticity also responds to other situations like stimulus from the environment. Neuroplasticity is observed during periods of learning as the brain changes structurally. As an individual learns, the internal structure of existing nerve endings can change as the brain makes new links. The accumulation of knowledge is not possible without the memory; the hippocampus is a component of the brain that is responsible for long-term memory and spatial navigation (Parasuraman and Rizzo, 2008). It is able to mold and change based on exterior input. A study of the hippocampus of London taxi drivers and bus drivers presents remarkable data; the hippocampi of the taxi drivers are noticeably larger than that of the bus driver’s (Parasuraman and Rizzo, 2008). Taxi drivers need to memorize the many roads of London in order to navigate efficiently whereas the bus drivers have a limited set of routes. Hence, the taxi driver’s need to learn and memorize the map of London reflects the experience of the navigating the city. As an individual learns, the internal structure of existing nerve endings can change as the brain makes new links. Furthermore, the size of the posterior hippocampus increased “…while the anterior hippocampus decreased in volume the longer the time taxi driving (Parasuraman and Rizzo, 2008).” These results suggest two things: the posterior hippocampus is more involved in long-term memory and spatial navigation and that neurons in the anterior hippocampus shifted to the posterior hippocampus during the reorganization of the brain’s circuitry. The results from the magnetic resonance imaging of the hippocampus indicate that experience and learning affects the shape of the brain. The brain’s shape can change other than having neurons move to another area—neurogenesis changes brain shape by generation new neurons. Neurogenesis can occur in adult human brains which proves that this organ does have the capacity to produce neurons after development. However, neurogenesis does not occur randomly; there is logic to the circuitry of the adult brain. The brain will only produce more cells in response to a stimulus. In the case of Huntington’s disease, a neurodegenerative disease, examinations of post mortem brains of individuals diagnosed with the disease reveal that “the degree of [neurogenesis] correlates with the [severity] of the illness (Taupin 2006)…” Damage by HD acted as a catalyst for the formation of neurons to compensate for the dead brain cells. However, the rate of neurogenesis does not occur at a rate that would balance the loss of neurons. This study has provides evidence that cell death is a stimulating factor of neurogenesis and most of all, that neurogenesis is possible in adult humans. The analysis of hemispherectomy patients, the brain in periods of learning, and brains with Huntington’s disease all demonstrate the neuroplasticity is a factual concept. Recent research not only refutes that postnatal neurogenesis is not possible, but it allows for a greater understanding of the relationship between the physiology of the human brain and its health and function. The study of neuroplasticity holds enormous potential; it can lead to treatments for stroke, post surgery therapies, or even cures for neurodegenerative diseases. The key to neurogenesis can possibly provide the key to many medicines in the future. Further study of neuroplasticity and neurogenesis will allow for a clearer understanding of the intricate and multifaceted adult human brain. The understanding of the brain’s capabilities and features is the gateway for later scientific discoveries. Works Cited Machado C. 2007. Brain Death: a Reappraisal. New York: Springer Publishing. Parasuraman R. and Rizzo M. 2008. Neuroergonomics: the Brain at Work. Oxford: Oxford University Press. Shaw C., McEachern J. C., and McEachern J. 2001. Toward a Theory of Neuroplasticity. London: Psychology Press. Taupin P. 2006. Adult Neurogenesis and Neural Stem Cells in Mammals. Hauppauge: Nova Publishing. Woolf CJ., Shortland P, and Coggeshall R. 1992. “Peripheral Nerve Injury Triggers Central Sprouting of Myelinated Afferents.” Nature Publishing Group. 02 January 1992. Web.23 November 2010. <http://www.nature.com/nature/journal/v355/n6355/abs/355075a0.html>
