Neuroplasticity, Its Types And Functions In Human Brain
Neuroplasticity is defined as the dynamic process of the brain where (by direction of the nervous system) it adapts to the requirements of the environment. The process consists of numerous neurobiological processes; comprising of physiological, metabolic, and structural mechanisms. Neuroplasticity can be further sub-grouped into functional (or neurologic) recovery, which is specifically after trauma, for example a stroke. It is also often discussed in conjunction with neurogenesis. Although similar, they are separate neural processes, where neurogenesis is the formation and rewiring of new connections - how newborn neurons are formed.
The brain is constantly undergoing change; the number of synaptic connections varies between the stages of life as the brain experiences synaptic pruning. Synaptic pruning is the elimination of unused synaptic connections, and the strengthening of regularly used connections; . It is beneficial for energy conservation and efficiency. This occurs as neurons travel down the neuronal axons until they reach their genetically predetermined destination. Once this happens the neurons compete with each other. The winning neurons are given trophic factors so that they survive whereas the defeated neurons die by cell apoptosis, thus i. It accounts for the loss of synapses in the brain.
By the time an infant is 3 years of age, the brain has reached its highest number of 15,000 synaptic connections. However, after synaptic pruning, an adult brain has approximately half the amount. Due to this, it was previously hypothesised that an adult brain is incapable of neuroplasticity, as it was believed that there is a neural “‘critical period”’ that an adult brain is beyond. Furthermore, it was also considered to be a “non- renewable organ”, within which there was a limited number of neurons which decreases throughout years. Nonetheless, recent research has proven these theories to be incorrect. It has since been discovered that the number of brain cells actually increases, throughout childhood especially. Two types of neuroplasticity exist. These are functional neuroplasticity and structural neuroplasticity. Functional neuroplasticity refers to the brain being able to allocate the function of a damaged region to an intact region. This is shown through recruitment of homologous areas when similar areas of the brain, possibly on the opposite side, take over the role(s) of the damaged area.
Structural neuroplasticity is when the brain’s structure physically changes from learning. This is evidenced through Maguire et al.’s study with London taxi drivers. Maguire et al (2000) conducted a study in which 16 male London taxi drivers were given an MRI scan and were found to have a significantly larger volume of grey matter in their posterior hippocampus, responsible for spatial and navigational skills, than in the control group of 50 non-taxi driving males. This shows structural plasticity as taxi drivers have to learn all the quickest routes around the city, so the compensation for the exertion extreme effort on the brain resulted in the larger volume of the posterior hippocampus.
Moreover, there was a positive correlation between amount of time the drivers had been in this career doing this job and the volume of grey matter. This further shows the effects of structural plasticity. Along with the recruitment of homologous structures, neuroplasticity occurs in three other ways; compensatory masquerade, cross-modal reassignment, and map expansion. Whereas more specifically, functional recovery occurs in two other ways: axonal sprouting, and the reformation of blood vessels. Compensatory masquerade is simply when the brain seeks an alternative method of performing a task. Cross-modal reassignment is the redirection of different inputs to a region of the brain, which due to damage, is not receiving its usual form of input. For example, an individual with visual impairment from birth may have input from their somatosensory area in their visual area (V1). Lastly, map expansion refers to the flexibility of brain areas specific for one neural function. The arrangement of neural region functions is described as a map.
Axonal sprouting is the regeneration growth of new nerve endings (neurogenesis) to reconnect to damaged neurons. Reformation of blood vessels occurs to increase blood flow to areas of the brain needing it the most.Recently, the neurotransmitter GABA has been cited as a possible future pharmacological therapy to aid in stroke (functional recovery). The brain region next to the area that experiences the stroke is called the peri-infarct zone; in a scientific study, GABAA receptor- mediated tonic inhibition was monitored and found to increase in this zone in mice after stroke. Following this, the researchers then administered GABA agonists to the mice, which moderated tonic inhibition. This resulted in an improvement of motor abilities within the mice as the drugs promoted GABAergic signalling and thus helped with cortical plasticity.
Conversely, it was also found that decreasing GABA inhibition too soon after the stroke actually increased stroke volume. Despite the fact that neuroplasticity is often seen as a beneficial process, there is such a thing as maladaptive neuroplasticity. This presents itself in phantom limb syndrome. Phantom limb syndrome is where an individual has undergone amputation for a limb but feels sensation in its place as if it is still there. Map expansion neuroplasticity has been suggested as a possible explanation for phantom limb syndrome. This is because, in neural studies it has been found that maps from one area shift to maps of the amputated area. As a result, the brain still acts as if a limb is there and neural activity will continue, thus resulting in either painless or painful sensations.
The brain-derived neurotrophic factor (BDNF) has become apparent as a key element in neuroplasticity. BDNF increases calcium ion influx into the neurons and exposition of receptors on the neurons. This, in turn, will trigger the activation of more neuronal pathways making for more effective neural function. It is known that aerobic exercise increases BDNF, and cortisol decreases BDNF levels. With this information, in the upcoming years, the stimulation of neuroplasticity is aimed to be used as a treatment for many neuro-degenerative disorders, such as schizophrenia, PTSD, Alzheimer’s etc.
Bibliography
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