Module 2
Lesson 1
by Dr. Irena O’Brien, PhD
Neuroplasticity
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Welcome to Module 2 on neuroplasticity, or how the brain rewires itself as a result of experience. Let’s begin with a short video.
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Neuroplasticity
How did you enjoy the video? Pretty amazing, isn’t it? This research is foundational. We saw that the hippocampi of the taxi drivers had increased in volume as they had more experience with London streets. And that’s one of the conditions of neuroplasticity, repetition, and the more repetition, the larger the hippocampus. We’ll come back to the London taxi drivers later on.
Neuroplasticity is a concept in neuroscience referring to the fact that the brain can actually "re-wire" itself as a result of environmental inputs. The change can be adaptive, as we saw with the London taxi drivers, or maladaptive. An example of a maladaptive change is phantom limb pain where the cortex is reorganized following the amputation of a limb. And in phantom limb pain, the pain is felt as if the limb were still there.
But the brain is not infinitely plastic, and to what extent it is an open question.
It was originally thought that the brain develops during a critical period in early childhood, then remains relatively unchangeable (or "static") afterward. It’s only in the last 50 years or so that we’ve come to realize that the brain can change based on experience. In addition, brain functions are not confined to specifically defined areas but harness many areas. This is important because if one brain area is damaged, say following a stroke, another brain area may take over some or all of the lost function.
Neuroplastic change can occur at small scales, such as physical changes to individual neurons, or at whole-brain scales, such as cortical remapping in response to injury; however cortical remapping only occurs during a certain time period meaning that if a child were injured and it resulted in brain damage then cortical remapping would most likely occur. However if an adult was injured and it resulted in brain damage, then large scale cortical remapping is less likely to occur since the brain has made the majority of its connections and plasticity declines with age. So, for example, if an adult were to lose their language abilities, it’s unlikely that the language areas of the brain would be remapped onto another structure.
Behaviour, environmental stimuli, thought, and emotions may also cause neuroplastic change, which has significant implications for healthy development, learning, memory, and recovery from brain damage.
By the way, this a brainbow of the adult cerebellum from a mouse that has been genetically modified to express several fluorescent proteins.
Image By Iris Salecker, Michael Häusser, and Mario de Bono [CC BY 3.0 (http:// creativecommons.org/licenses/by/3.0)], via Wikimedia Commons
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Sensory Homunculus
We saw in the first module how sensory information from different body parts project to different areas on the brain so that, for example, the cortical site for the elbow is different from the cortical site for the tongue.
An early study looked at the impact of removing body parts on the cortical map. Michael Merzenich and colleagues removed the third digit in owl monkeys. Before amputation, there were five distinct areas in the somatosensory cortex, one for each digit. Sixty-two days after the amputation, the cortical area originally occupied by the third digit was invaded by the areas occupied by the two adjoining digits, digits 2 and 4. Decades of research have found that injuries that begin in the body result in reorganizational make-overs of the entire core of the somatosensory brain, from peripheral sensory neurons to the cortex. So it’s not just the brain itself that’s affected, but the entire nervous system.
Paul Bach-y-Rita was a pioneer in neuroplasticity research. He helped blind people see in a radically different way, through vibrations on the skin. And the remarkable thing was that the information from their skin was processed in the visual cortex, located in the occipital lobe at the back of the brain. How he came to be a neurologist and study neuroplasticity is a fascinating story. And this next video can tell it better than I.
Merzenich, M.M.; Nelson, R.J.; Stryker, M.P.; Cynader, M.S.; Schoppmann, A.; Zook, J.M. (1984). "Somatosensory Cortical Map Changes Following Digit Amputation in Adult Monkeys". Journal of Comparative Neurology. 224 (4): 591–605. doi:10.1002/cne.902240408
Wall, J.T.; Xu, J.; Wang, X. (September 2002). "Human brain plasticity: an emerging view of the multiple substrates and mechanisms that cause cortical changes and related sensory dysfunctions after injuries of sensory inputs from the body". Brain Research Reviews. Elsevier Science B.V. 39 (2–3): 181–215. doi:10.1016/S0165-0173(02)00192-3
Image by OpenStax College - Anatomy & Physiology, Connexions Web site. http://cnx.org/content/col11496/1.6/, Jun 19, 2013., CC BY 3.0, https://commons.wikimedia.org/w/index.php?curid=30148008
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https://vimeo.com/59755393
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Neuroplasticity starts in the womb
This is an amazing story! It was the beginning of research into neuroplasticity and showed that structural brain change was possible through consistent effort over a period of time.
Brain structure and function, and even the expression of genes, are all interactive, meaning that they are influenced by experience as well as vice versa. They also influence experience.
And this starts in the womb where environmental influences, such as the diet of the mother and the presence of viruses or toxic agents, alter brain structure and, hence, function.
Following birth, all of our everyday experiences result in tiny changes in the structure of our brain, in the form of altering the pattern of synaptic connections.
And the contemporary notion of “environment” is far broader than is commonly understood. It includes biological circumstances, such as diet, exposure to toxins, as well as personal and social circumstances.
During childhood, there is a constant interaction between environment and genetic factors, with a mature cognitive system emerging out of transformations of earlier ones.
At birth, the brain is small - 450 g relative to the adult size of 1400 g. The vast majority of neurons are formed prior to birth, so the expansion in brain volume during postnatal development is due to factors such as the growth of synapses, dendrites, and axon bundles, the proliferation of glial cells; and the myelination of nerve fibres. Glial cells are non-neuronal support cells.
The formation of synapses (synaptogenesis) rises and falls as the brain matures. In the prefrontal cortex, for example, the peak is reached after 12 months, but does not return to adult levels until 10 - 20 years of age. The decrease in synapses is known as synaptic pruning and represents a process of fine-tuning to the needs of the environment, which renders some connections redundant.
Myelination refers to the increase in the fatty sheath that surrounds axons and increases the speed of information transmissions. The increase in white matter volume over the first two decades of life may reflect the time course of myelination. The prefrontal cortex is one of the last areas to achieve adult levels of myelination, and this, together with the late fine-tuning and elimination of synapses in this region, may contribute to the development of mature social behaviour during adolescence and the control of behaviour in general.
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