NEUROPLASTICITY AND FUNCTIONAL RECOVERY OF THE BRAIN
INTRODUCTION TO BRAIN PLASTICITY
“Neuroplasticity refers to the physiological changes in the brain that happen as the result of our interactions with our environment. From the time the brain begins to develop in utero until the day we die, the connections among the cells in our brains reorganize in response to our changing needs. This dynamic process allows us to learn from and adapt to different experiences”
— Celeste Campbell (n.d.).
KEYWORDS BRAIN PLASTICITY
Brain plasticity, or neuroplasticity, is an umbrella term that describes the brain’s changeability throughout a species’ lifetime. The brain’s structure is not static and fixed; it is an organ that constantly alters its configurations and functions and reorganises neural pathways throughout the lifespan due to experience. Many types of brain cells are involved in neuroplasticity, including neurons, glia, and vascular cells.
Neuroplasticity does not consist of a single type of change, but rather includes many different types, for example, developmental plasticity, structural plasticity, and functional plasticity - however, some of these types cross over and/or have similar processes.
NEUROGENESIS:
Neurogenesis replaces neurons that have died. It has recently been found that Contrary to popular belief, a minority of neurons are continuously made in specific regions in the adult brain and the developing brain (OECD, 2202). This process is known as Neurogenesis- e.g., the process by which neurons are generated from neural stem cells and progenitor cells or to put it more simply, the growth and development of nervous tissue.
It should be noted that developmental neurogenesis and adult neurogenesis differ markedly and that most neurogenesis occurs prenatally. Neurogenesis has massive applications in the treatment and prevention of dementia and recovery from traumatic brain injuries.
NEUROPLASTICITY VERSUS NEUROGENESIS
Although similar, neuroplasticity and neurogenesis are two different concepts. Neuroplasticity is the ability of the brain to form new connections and pathways and change how its circuits are wired; neurogenesis is the even more amazing ability of the brain to grow new neurons
SYNAPTOGENESIS:
is the formation of synapses between neurons in the nervous system (e.g. change in the internal structure of the neurons, the most notable being in the area of synapses and/or an increase in the number of synapses between neurons).
EXUBERANT SYNAPTOGENESIS
Although synaptogenesis occurs throughout a healthy person's lifespan, an explosion of synapse formation occurs during early brain development when the immature brain first begins to process sensory information through *adulthood (*approx. 25 years of age).
NEURAL MIGRATION:
Neuronal migration is the method by which neurons travel from their origin or birthplace to their final position in the brain, in other words, it is the process of organising the brain by moving neurons to specific areas based on the functions these cells will perform. Migration begins prenatally but continues after birth.
MYELINATION OF NEURONS:
Myelin is a fatty white substance that surrounds the axon of some neurons, forming an electrically insulating layer. The main purpose of a myelin layer (or sheath) is to increase the speed at which impulses travel along with the myelinated fibre. Myelination is the process of coating the axon of each neuron with a fatty coating called myelin, which protects the neuron and helps it conduct signals more efficiently. Myelination begins in the brain stem and cerebellum before birth but is not completed in the frontal cortex until late adolescence. Breastfeeding contributes to more rapid myelination in the brain.
AXON SPROUTING:
New nerve endings grow and connect with undamaged areas. Neuronal unmasking: The unmasking of neural pathways and synapses which are not normally used for the particular function under study but which can be called upon when the ordinarily dominant system fails.
SYNAPTIC PRUNING:
Synaptic pruning or axon pruning is the process of synapse elimination that occurs between early childhood and the onset of puberty in many mammals, including humans. Pruning occurs to weed out unnecessary connections and strengthen the important ones based on the child's experiences. Pruning provides room for the most important networks of connections to grow and expand, making the brain more efficient. Some pruning begins very early in development, but the most rapid pruning happens between about age 3 and age 16 (Pruning can also occur beyond 25 years). Different areas of the brain undergo pruning during different sensitive periods. Pruning is a process that is more important than was once believed. Experiences during infancy and childhood form the connections that shape the development of the brain.
CRITICAL PERIOD:
In developmental psychology and developmental biology, a critical period is a maturational stage in the lifespan of an organism during which the brain is especially sensitive to certain environmental stimuli. It has been hypothesised that if, for some reason, the organism does not receive the appropriate stimulus during this "critical period" to learn a given skill or trait, it may be difficult, ultimately less successful, or even impossible, to develop some functions later in life.
SENSITIVE PERIODS:
Sensitive periods refer to opportunities for types of learning that are less precise and cover a longer period compared to the critical period. During this period, if there is a lack of opportunity for a certain type of learning, it is not gone forever (as it is for critical periods). Skills can still be acquired later in the individual’s lifespan.
EXPERIENCE-EXPECTANT PLASTICITY AND EXPERIENCE-DEPENDENT PLASTICITY:
The brain is the definitive organ of adaptation. It takes in information and choreographs complex behaviours that enable individuals to act in sometimes spectacular, sometimes appalling ways. Most of what people think of as the “identity”—what we consider, what we recall, what we can do, how we sense—is learned by the brain from the experiences that occur after birth. Some of this information is acquired during critical or sensitive periods of development when the brain appears ready to take in specific kinds of information, while other information can be acquired across broad periods of development that can extend throughout the lifespan. This range of possibilities is documented by corresponding research of both the remarkably rapid brain development that characterises the early childhood period (EXPERIENCE-EXPECTANT PLASTICITY) and the brain's lifelong capacity for growth and change (EXPERIENCE-DEPENDENT PLASTICITY). The balance between the lasting significance of early brain development and its continuing plasticity lies at the centre of the current debate about the effects on the brain of early experience.
DEVELOPMENTAL PLASTICITY
SYNAPTOGENESIS
It is now believed that the majority of the neurons that will eventually comprise the human brain are formed in the womb and are present from birth. By birth, the brain has developed around a hundred billion neurons, but most of these neurons only have rudimentary networks, e.g., the connections to other neurons are fragile or have not yet been formed. Almost instantly after birth, the newborn’s brain creates trillions of connections and pathways between the neurons. What changes most dramatically is the growth of dendrites and axons and the number of synapses connecting neurons, - seven hundred new neural connections every second; this is known as exuberant synaptogenesis.
The developing brain is especially sensitive to a broad range of experiences, showing an extraordinary capacity for plasticity that influences behavioural changes throughout the lifetime.
WHY ARE HUMAN BABIES BORN PREMATURE?
Humans are not that different from kangaroos because, like them, we have been naturally selected to deliver our babies prematurely. The human brain is not a complete organ at birth. Indeed, by one assessment a human foetus would have to undertake a gestation period of eighteen to twenty-one months instead of the usual nine to be born at a neurological and cognitive development stage comparable to that of a chimpanzee neonatal. The human brain needs at least twelve years for broad development and twenty to twenty-five years for full development.
HUMANS ARE BIPEDAL AND HAVE NARROW HIPS COMPARED TO A CHIMPANZEE
THEORY ONE
The traditional explanation for the nine-month gestation period and helpless newborn is that natural selection favoured childbirth at an earlier stage of foetal development to accommodate a brain size that could fit through the narrower hips that resulted from bipedalism.
THEORY TWO
The second theory suggests the metabolic demands of a human foetus threaten to exceed the mother’s ability to meet both the baby’s energy requirements and her own. Think how much food a baby needs at nine months gestation and remember the hostile ancestral environment humans emerged from. As a result, mothers may have been forced to deliver their babies early to avoid starving,
An Artist’s Impression of our Ancestral Environment
THEORY THREE
The third theory suggests that humans are born with blank brains as it enables the nervous system to escape the restrictions of its genome and to become adaptive to all the environments and situations that humans might encounter, say from living in the Arctic and eating mainly meat, to living in the desert and being vegetarian for example. Other animals have less need for such plasticity as they have evolved to only flourish in one type of environment. A rhino, for example, can’t thrive anywhere but in a hot arid environment, because its brain is fixed at birth, it can’t learn new stuff. But a human can live and adapt to any climate, language or way of life.
Whatever the reason, human babies are born so early that their brains are less than thirty percent of their adult brain size, they are effectively premature.
EXPERIENCE DEPENDANT PLASTICITY ALSO KNOWN AS DEVELOPMENTAL PLASTICITY
Experience-expectant plasticity is when the brain expects to have certain experiences, e.g., seeing a face, before it can wire up correctly. Experience-expectant plasticity is typified by neurogenesis, synaptogenesis exuberant synaptogenesis, synaptic pruning, neural migration, and the myelination of neurons that are prolific during the first few years of life.
The brain is not fully matured at birth, and this may be because humans need their brains to develop in a culturally specific way to navigate their environment successfully. During the early years, the brain creates many connections and pathways. The recurrence of an action or experience helps to carve these pathways into the brain. Once they have become strengthened adequately, they become permanent.
Experience-expectant plasticity refers to the integration of specific environmental stimuli into the normal patterns of development. Certain environmental exposures are needed during limited critical or sensitive periods in a baby’s development and are essential for healthy maturation. For example, finches need to hear adult songs before sexual maturation for them to learn to sing at a species-appropriate level of intricacy. Humans need to experience hearing language or seeing faces during critical stages of their cortex’s development. If they do not receive the correct stimuli then this area may be pruned away after the first six months of life.
In short, experience-expectant plasticity is the generalised development of neuron connections that occur due to common experiences that all humans are exposed to in a normal environment. It is thought that the human brain evolved to start life with an innate desire to wire up specific sensory experiences: For example, faces to enable face recognition, visual-spatial information for navigation; specific voices for language acquisition,
CRITICAL PERIODS
Experience expectant plasticity is tied to the concept of a critical period.
Experience-expectant plasticity is when the brain has heightened sensitivity to sensory information that is compulsory for developing a particular skill e.g. certain areas of the visual cortex are only capable of normal growth during the first few months of life. Experience-expectant plasticity always occurs during early postnatal development. During a critical period. The critical period is the notion of a window of opportunity opening in early childhood, and then closing, never to open again. For instance, a child raised hearing Korean will thus be exposed to different speech sounds than a child raised in an English-speaking environment. Early in life, infants can discriminate the speech sounds of all languages, but over the first year, the auditory system begins to change such that the infant becomes expert in discriminating sounds in its language environment but loses the ability to discriminate sounds that are not experienced.
Once the critical period has elapsed if an individual has not been exposed to the necessary stimuli, the individual will have some impairment and brain development will proceed abnormally. This is because from early childhood until late adolescence, the brain begins to prune some of these connections. Those connections that are not sufficiently strong, have been neglected or are used infrequently are lost; “use it or lose it”. In other words, if a child is deprived of language or seeing faces, their brains will lose the capacity to use this function, and they will become mute or face blind for life! By the age of 18, experiences that are not revisited are lost, and the number of connections has been reduced to around 500 trillion - the same number the young adult had as an 8-month-old.
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Thus, normal brain development depends on exposure to expected sensory experiences like hearing a language and seeing faces because these sensory inputs are necessary for neural connections to form in the areas of speech and face recognition. Abilities that have a critical period are functions that the brain could expect to use, such as being visually spatially aware. Forming connections and pathways in these areas is crucial as they enable a person to see, hear, smell, learn and reason. For example, at birth, although basic circuits concerning vision are in place, the circuitry is rudimentary, so a baby's vision is pretty fuzzy - they can make out light, shapes, and movement. They can see only about eight to fifteen inches away. A baby's vision will develop further through the early visual experiences gained during certain periods of its development, e.g., what a baby visualises during the weeks after birth.
Different circuits wire up at different times during infancy – smiling occurs at about six weeks, walking at twelve months, and object permanence at around nine months.
RESEARCH SUPPORT
DEPRIVED ENVIRONMENTS
The critical window and pruning are supported by experiments, for example, rearing animals in deprived environments thwart development and may lead to the permanent loss of function. Monkeys, cats, or rats raised in the light but without patterned visual stimulation show poor visual behaviour guidance, even after prolonged recovery periods with patterned visual input. The reduced vision is associated with reduced dendritic branching.
A study on visual deprivation in cats in which one eye of newborn kittens was fixed shut for three months (Wiesel & Hubel, 1965). After this time the researchers studied the connections between the two eyes (‘open’ and ‘shut’) and the brain. They found that there was a severe deterioration of neuronal connections in the visual areas of the brain’ because of lack of stimulation of the closed eye. The brain had, in effect, wired itself to receive information only from the open eye and remained blind in the other eye (Blakemore & Frith, 2000). When adult cats were subjected to a similar period of visual deprivation in one eye, there was no deterioration in neuronal connections because they had wired up both eyes for vision when they were kittens. The conclusion was that the visual system requires sensory input at a critical period of development (usually the first months of life) if it is to ‘wire itself up’ to perceive its environment.
Clearly, comparing cats with humans is not always helpful as their visual systems have developed as a response to different selective pressures, so cats cannot recognise faces and cannot see in colour, but they have better peripheral vision than humans, for example. However, cases of blind people who regain sight in adulthood show how they are always face-blind. Others, with less severe, early visual deprivation, may have trouble differentiating between male and female faces or be unable to decipher emotion from facial expression.
PARENT-CHILD RELATIONSHIPS
New synaptic connections and the maintenance of existing connections occur in response to social experiences. That is, the development of an infant’s brain, depends on meaningful forms of sensory and motor stimulation from caregivers. This stimulation includes emotional interactions with responsive caregivers.
Three findings in child development neuroscience have relevance for plasticity:
The special sensitivity of brain development to supportive experiences with people.
The dependence of the developing brain on social and emotional inputs for the establishment and retention of synaptic connections.
The “conditioning” of the brain by experiences in the nurturing relationship with caregivers, especially about stress-reactivity.
High-energy growth spurts in the brain during early childhood are embedded in and regulated by the emotional interchanges between infants and their caregivers (Siegel, 2001). Siegel argues that there is a great deal of agreement across several fields of research in different disciplines, in both animal and human studies, pointing to the cardinal importance of emotional communication to the development of the brain.
These early brain developments can be halted or distorted by an absence of experience-dependent neurochemical cues when expected experiences do not occur, as in an emotionally deficient caregiving environment. They can also be damaged by cues that are abnormal, as might occur in maltreatment. In the latter case, brain development is affected by the presence of high quantities of the hormone cortisol produced by the hypothalamic-pituitary-adrenal-cortical system during long periods of stress.
As examples of evidence for these claims, Greenough and Black (1992) found that dendritic growth in rat pups is dependent on particular forms of tactile and emotional stimulation during nursing. In human infants, interpersonal encounters involving mutual gaze start to peak at about 2 months of age. They are associated with dramatic metabolic changes in the primary visual cortex, during which the infant’s visual experiences modify synaptic connections in the occipital cortex (Katz, 1999).
In rat studies, early experiences in mother-pup interactions have been found to permanently alter the stress-reactivity of the rat pup’s brain. Removing the mother from her pups for regular periods each day disrupts the mother’s nurturant behaviour. This produces long-term changes in the stress-reactive hormonal and behavioural responses in her pups. In contrast, handling and tactile stimulation associated with comforting experiences, which the mother rat provides to the pup, induce permanent modifications in stress hormones in the hypothalamus (Schore, 2001a). Rat pups exposed to these supportive rearing conditions are less anxious and fearful and less stress-reactive in later life.
If the results of these animal studies can be extrapolated to human infants, and many people working in this field think the findings are relevant, it has to be concluded that the emotional and social qualities of early experiences are significant because they have permanent effects on the child’s brain. The effects occur either through experiences that fulfil or don’t fulfil the experience- and use-dependent development of the brain and its neuronal connections, or by conditioning the brain to respond to environmental conditions, especially stress, in ways that strongly program later behavioural responses. High stress-reactivity causes cognitive disruption and high levels of emotionality, which interfere with intellectual and social functioning (Shonkoff & Phillips, 2000).
Young mammals depend on their parents and must learn to identify, remember, and prefer their caregivers. Modifying these relationships can significantly alter brain development and leave effects that remain into adulthood. For example, extensive studies on rats have shown that the time spent in contact between the mother and pups, including both the amount of maternal licking and grooming, correlate with a variety of somatic and behavioural differences, and especially modify the development of the hypothalamic-pituitary-adrenal axis. These changes are correlated with changes in gene expression in the offspring. Other studies have shown changes related to maternal-infant interactions in the mPFC, OFC, hypothalamus, and amygdala.
The effects of reduced parent-child interactions in humans have been studied in children adopted from institutions and related to the age at adoption. For example, 12- to 14-year-old children who were adopted from institutional care at a mean age of 12 months had reduced grey-matter volumes and especially reduced prefrontal volume, which was consistent with previous studies showing reduced prefrontal cortical thickness (e.g. Hodel et al.17). Extensive studies of Romanian orphans adopted to various Western countries have shown similar results, although one additional finding is that adoption after about 18 months is associated with very poor behavioural and neurological outcomes, even after over 20 years of living in good and stable families. These children have smaller than normal brains, reduced cognitive and social functions, and abnormal brain electrical activity (e.g. Johnson et al.).
Romanian Institution
Chugani et al. (2001) administered PET scans to a sample of 10 children adopted from Romanian orphanages and compared them with 17 normal adults and a group of 7 children. Assessments showed mild neurocognitive impairment, impulsivity, and attention and social deficits. Specifically, the Romanian orphans showed significantly decreased activity in the orbital frontal gyrus, parts of the prefrontal cortex/hippocampus, the amygdala and the brain stem. Chugani concluded that the dysfunction in these brain regions may have resulted from the stress of early deprivation and might be linked to long-term cognitive and behavioural deficits.
Romanian Institution
LANGUAGE, COGNITIVE EXPERIENCE, AND POVERTY
Infants can discriminate the speech sounds of all languages over the first year, but the auditory system begins to change such that the infant becomes an expert in discriminating sounds in its language environment but loses the ability to discriminate sounds that are not experienced. Learning more than one language in development adds another dimension, and especially in learning how to switch routinely between languages. This mental switching has a significant impact on cognitive abilities, especially in enhancing attentional and executive functions and in increasing cognitive reserve in ageing, presumably by some plastic change in the frontal lobe.
FACTORS THAT AFFECT BRAIN PLASTICITY
Although virtually all children learn a language, there are large differences in the rate of vocabulary acquisition. In a powerful study, Hart and Risley followed children for two and a half years (from the age of 7–9mo to 36mo) by observing the families at home for 1 hour each month.11 Children could be grouped into those with large vocabularies at three years of age (~1200 words) versus those with smaller vocabularies (~400–600 words). This difference was related to the number of words that the children had been exposed to in the home, which was directly related to socioeconomic status (SES). Thus, over one year, children of high SES would have been exposed to about 11 million words and children of low SES to about 3.2 million words. By four years of age, the average child of lower SES would have been exposed to about 30 million fewer words than the child of higher SES. When the children were measured again at 9 to 10 years, the SES-related difference actually grew larger, suggesting that school had a negligible effect in erasing this deficit.
The SES-related difference in cognitive abilities is related to developmental differences in the cerebral cortex. Noble et al.12 examined the relationship between SES and cortical surface area in over 1000 participants between the ages of 3 years and 20 years. Lower family income, independent of ethnicity or sex, was associated with decreased cortical surface area in widespread regions of the frontal, temporal, and parietal cortex, and this was correlated with poorer performance on tests of attention, memory, vocabulary, and reading. Thus, lower SES is associated with a smaller cortical surface area and poorer test outcomes.
Most research on nutrients in development has focused on the effects of nutrient deficiencies, especially related to protein-energy, iron, zinc, copper, and choline. Such nutritional deficiencies can have global effects on the developing brain or brain circuit-specific effects, depending upon the precise timing of the nutrient deficit. A more intriguing question is whether brain plasticity might be enhanced by vitamin and/or mineral supplements, and especially a combination of nutrients that would work synergistically to enhance metabolic activity and, ultimately, brain functioning. One promising product is EmpowerPlus. This product is a blend of 36 vitamins, minerals, and antioxidants, and includes a proprietary blend of herbal supplements such as ginkgo Biloba and the amino-acid precursors for neurotransmitters, choline, phenylalanine, glutamine, and methionine. This product has been reported to improve mood and behaviour in children and has been shown to decrease anger, activity levels, and social withdrawal in autism while also increasing spontaneity. Rodent studies have shown that using this supplement during development leads to enhanced motor and cognitive functions and increased dendritic arbour in mPFC. The mechanism of dietary effects on the neuronal structure may be epigenetic. Dominguez-Salaz et al.25 studied gene methylation in the blood of infants conceived either in the Gambian dry or rainy season. The maternal diets are dramatically different in the two seasons and so was the pattern of gene methylation.
GUT BACTERIA
Given that the microbiome interacts with the brain, Dinan et al.26 proposed that the use of bacteria to alter the microbiome could be a novel class of psychotropics, which are called psychobiotics. The idea is that manipulation of bacteria in the gut could modify brain plasticity, a conclusion supported by several studies showing that normal gut microbiota can affect the brain and behavioural development. For example, manipulation of gut bacteria in newborn mice influenced motor and anxiety behaviours. These behavioural changes were correlated with changes in the turnover of noradrenaline, dopamine, and serotonin in the striatum, as well as changes in the production of synaptic-related proteins in the cortex and striatum.
IMMUNE SYSTEM
Many proteins in the immune system are expressed in the developing brain and some appear essential for the development and modifications of synapses. Although there is little direct evidence that the immune system can compromise brain development and plasticity, epidemiological evidence implicates maternal infection as a risk factor in various neurodevelopmental disorders, including autism, attention deficit–hyperactivity disorder, and schizophrenia.
OTHER A03:
There has been much publicity about how plasticity can enable anybody to learn anything regardless of age or past educational deficits, however, this is only true for experience dependant learning and not experience expectant. This means that policymakers should ensure that children from impoverished backgrounds receive very early interventions in their care and education as investing in social care or education beyond the window of 6ths - 2 years will be too late to repair inequalities.
It is theorised that the more resistant types of learning that are often seen in adult samples are a result of EXPERIENCE EXPECTANT PLASTICITY, e.g., faces, language learning to categorise (first schema template), number-sense, time-sense, deception, social-relations, and positive-self-schema things the brains need to operate normally, regardless of location.
CONCLUSIONS
The developing brain is responsive to a wide range of factors that modulate its development beginning with preconception experiences of the parents, gestational experiences, and postnatal experiences. We have considered these factors as though they are independent singular events, but as we go through life experiences interact to alter both behaviour and brain, a process often referred to as meta-plasticity. We have only just begun to understand how different factors might interact with one another or how the effects of negative factors, such as severe stress, might be ameliorated by experiences such as tactile stimulation. We have focused here on changes in behaviour, neuronal morphology, and epigenetics, but we certainly recognize that plastic changes in brain organization can be studied at many other levels in both humans and laboratory animals. Finally, in our discussion, we have given equal weight to each factor, but there are likely significant differences in the magnitude of the effects. The effects of early stress and psychoactive drugs are the most studied negative effects and likely the most powerful. On the positive side, early experiences such as tactile stimulation would appear to be very influential and can reverse some of the negative effects of stress and perhaps psychoactive drugs.
STRUCTURAL PLASTICITY
NEUROPLASTICITY: EXPERIENCE-DEPENDENT PLASTICITY ALSO KNOWN AS STRUCTURAL PLASTICITY (OPERANT AND CLASSICAL CONDITIONING ARE INCLUDED HERE)
The critical window was once the basis for the belief that the older brain could not acquire a new skill without many difficulties. The hypothesis that behaviours are acquired during a critical period was first proposed by neurologists Wilder Penfield and Lamar Roberts in 1959 and popularised by linguist Eric H. Lenneberg in 1967. Lenneberg argued for the hypothesis based on evidence that children who experience brain injury early in life develop far better language skills than adults with similar injuries.
But it is now believed that the reason why some types of learning are more resistant to plasticity in older individuals but others are not is to do with how necessary the skills are to human development. Human brains didn't evolve to manifest many of the skills that are required in modern life – many of which are culturally relevant, for example, driving, writing, algebra, cooking, geography, etc. Humans are adaptable creatures they can live anywhere and have the potential to speak any language or learn a new skill. It makes sense then that the brain can learn new things throughout its lifespan.
EXPERIENCE-DEPENDENT PLASTICITY
Experience-dependent plasticity is also known as activity-dependent learning and structural plasticity.
Experience-dependent plasticity is the plasticity of learning and memory that occurs throughout life.
Specifically, it is a form of functional and structural neuroplasticity that arises from using cognitive functions in response to personal experience. Human beings need to constantly learn throughout their lifespan, and structural plasticity enables the human brain to adapt by learning, either operantly, classically or through imitation This enables people to acquire specific sets of expertise in many areas e.g. education, geographical knowledge, language, driving, cooking, etc,
Experience-dependent plasticity is the biological basis for learning and forming new memories.
INTRODUCTION
It was once believed that the adult brain's networks became fixed after a certain age, “ old dogs cannot learn new tricks”. In the past two decades, however, much research has revealed that the brain never stops changing, learning and adjusting to experience. This type of brain change is known as experience-dependent plasticity. In short, it refers to most skills and knowledge developed over the lifespan. It is called experience-dependent because the brain does not necessarily expect to learn what it is presented with, e.g., an Eskimo child learning how to build an igloo). These skills are probably acquired via, operant, classical and observational learning and help formulate schemas and semantic knowledge too. There is no critical period for experience-dependent learning e.g. you can learn how to drive when you are 16, 30 or 50. This may be why some older samples seemed to learn some skills very easily even if they had not been exposed to them in childhood. All of education is about experience-dependent plasticity.
The capacity of the brain to change with learning and the memorising of new knowledge is vital for survival as humans need to constantly learn new things so they can navigate their environments successfully. The brain’s ability to reorganise neural pathways throughout the lifespan results from experience. But, it refers to the brain’s ability to change with learning.
With EXPERIENCE-DEPENDENT PLASTICITY there is a change in the internal structure of neurons, notably, the number of synapses increases and dendrites and axons sprout more profusely.
RESEARCH
There have been several studies that have supported the fact that the adult human brain retains a degree of ‘plasticity’ – i.e. that its structure and organisation can physically change as a result of new demands placed upon it and that these changes can occur in adulthood and are not confined to a period of childhood development. One of these studies compared structural MRI scans of the brains of London taxi drivers with a group of control subjects who did not drive taxis (Maguire et al, 2000). It was found that ‘the posterior hippocampi of taxi drivers were significantly larger than those of control subjects and that the hippocampal volume correlated with the amount of time spent as a taxi driver.
EVALUATION:
Maguire’s study has many positives; it has real-world applications, and the control group allows for comparison. But the research is beta-biased, it doesn’t really tell us about plasticity in female brains, as the samples were male. Maybe the posterior hippocampi are more prone to plasticity in males because of the influence of Testosterone on visual-spatial memory, which is more often found in males. Moreover, taxi drivers cannot be generalised to the population as they have developed a high degree of specialised knowledge over a long period.
However, studies have also shown that unskilled individuals can learn a new skill remarkably quickly and that the physical evidence for this plasticity shows up very quickly. One study took a group of non-musicians and asked them to practice a set of five-finger exercises for the piano for two hours a day for five days. At the end of the five days, the part of their brain responsible for finger movement was found to be enlarged and more active compared to a group of control subjects who had not performed the exercises (Pascual-Leone et al, 1995).
Other studies of adult learning have included females and other types of learners. Work with musicians, for instance, discovered that part of the auditory cortex of skilled musicians was up to 25% larger than in non-musician control subjects and that the extent of the comparative enlargement was correlated with the age at which the musicians began to practice (Pantev et al, 1998).
Pantev’s results indicate there is also a natural decline in cognitive functioning with age.
One of the most popular theories to explain the decline of learning in older brains is synaptogenesis. It would appear from research findings that the younger an individual is, the more prolific and speedy the neural connections occur. Indeed, when synaptogenesis occurs in infancy, it is called exuberant synaptogenesis because of its productiveness. As the brain ages, synaptogenesis happens with less speed and frequency; maybe this explains why older people seem to learn some tasks more slowly.
There are other theories on the cognitive decline of the brain in older people. For instance, one theory suggests that older people may process and retrieve information and knowledge at a slower rate as they have too many neural connections making the speed of processing information and learning much slower. Indeed scientists from Tübingen University in Germany believe the human brain works slower in old age as it has to process a lifetime of stored-up information to recall simple facts (hence the more connections). They say their research proves instead of being weak - older brains are, in fact, more powerful. Maybe cognitive decline is more to do with the de-acceleration of synaptic pruning.
There is, however, research that shows that the brain carries on learning into old age. Boyke et al (2008) found evidence of brain plasticity in sixty-year-old participants who were taught a new skill – juggling. They found increases in grey matter in the visual cortex, although when the practising stopped, these changes reversed.
Imaging (e.g., fMRI, PET, MEG) studies of the developing human brain have confirmed that growth and development continue until early adulthood. Some areas, however, do seem less resistant to change. For example, music training for temporal patterns must happen early on in early development but perceiving and repeating tones can be learned at any age.
“In the brains of nine string players examined with magnetic resonance imaging, the amount of somatosensory cortex dedicated to the thumb and fifth finger of the left hand -- the fingering digits -- was significantly larger than in nonplayers. How long the players practised each day did not affect the cortical map. But … the younger the child when she took up an instrument, the more cortex she devoted to playing it. “ Newsweek, February 19, 1966
The Critical Period is the notion of a window of opportunity opening in early childhood, and then closing, never to open again and was the basis for the belief that the older brain could not acquire any new skill without much difficulty.
The hypothesis that behaviours are acquired during a critical period was first proposed by neurologists Wilder Penfield and Lamar Roberts in 1959 and popularised by linguist Eric H. Lenneberg in 1967. Lenneberg argued for the hypothesis based on evidence that children who experience brain injury early in life develop far better language skills than adults with similar injuries.
The reason why some types of learning are more resistant to plasticity in older individuals, but others are not may have to do with how necessary the skills are to human development. Human brains didn't evolve to manifest many of the skills that are required in modern life – many of which are culturally relevant, for example, driving, writing, algebra, cooking, geography, etc. It is theorised that the more resistant types of learning that are often seen in adult samples are a result of EXPERIENCE EXPECTANT PLASTICITY.
EXPERIENCE EXPECTANT PLASTICITY refers to a finite period in which an organism has heightened sensitivity to external stimuli that are compulsory for developing a particular skill, e.g. certain areas of the visual cortex are only capable of synapse formation during the early stages of development. Individuals MUST BE EXPOSED to external visual images or the synapses cannot link up and create pathways representing, for example, visual memories, spatial awareness, and face recognition. When these abilities develop, they generally recruit specific areas of the brain.
It is thought that the human brain evolved under the pressure of natural selection to have some abilities: basic vision, first language learning, categorisation, number sense, time sense, deception, and social relations.
Once the critical period has elapsed if an individual has not been exposed to the necessary visual stimuli, the individual will have some visual impairment. If they are absent, brain development proceeds abnormally, and critical period effects can occur. Brain development depends on the exposure to the relevant concepts e.g., the input that is necessary for these abilities are those that the brain could expect to encounter.
Other Supporting Evidence:
Playing video games
Playing video games makes many different complex cognitive and motor demands. Kuhn et al (2014) compared a control group with a video game training group that was trained for two months for at least 30 mins per day on the game Super Mario. They found a significant increase in grey matter in various brain areas including the cortex, hippocampus and cerebellum. This increase was not evident in the control group. The researchers concluded that video game training had resulted in new synaptic connections in brain areas involved in spatial navigation, strategic planning working memory and motor performance - skills that were important in playing the game successfully.
Meditation
Researchers working with Tibetan monks have been able to demonstrate that meditation can change the inner workings of the brain. Davidson et al (2004) compared eight practitioners of Tibetan meditation with ten student volunteers with no previous meditation experience. Both groups were fitted with electrical sensors and asked to meditate briefly. The electrodes picked up on the much greater activity of gamma waves (important because they coordinate neuron activity) in the monks. The students showed only a slight increase in gamma wave activity while meditating. The researchers concluded that meditation not only changes the workings of the brain in the short term but may also produce permanent changes, based on the fact that the monks had far more gamma wave activity than the control group even before they started meditating.
Wider implications of the research
The knowledge cleaned from plasticity research has many implications for society. Knowledge about how we learn has applications to educational theory, i.e., how people learn and why some people might find learning problematic (special needs education). Indeed much research has now been directed at ‘hot housing’ infants and/or looking at ways to increase synaptogenesis. The principle of creating enriched environments initially seemed to be backed up by research by Kempermann et al. (1998), who investigated rats who were brought up in either an ‘enriched’ or a ‘deprived’ environment. The ‘deprived’ environment was a normal laboratory cage for a single rat, while the ‘enriched’ environment included various toys such as wheels and ladders, and also had other rats for company. It was found that the rats brought up in the ‘enriched’ environment had up to 25% more synapses per neuron in brain areas involved in sensory perception than ‘deprived’ rats raised alone in a lab cage with no ‘playmates’ or toys. Furthermore, the rats raised in complex environments perform learning tasks better than deprived rats. (Blakemore & Frith, 2000).
Once again, one must be cautious as there are limitations when using animal studies the obvious point is that animals are not humans – they are less flexible in their behaviour and do not possess human higher-order skills. It is also known that the locations of certain processes in animal brains are different from those in human brains (e.g. rats and humans appear to use different parts of the brain for working memory), and that the brain matures differently in different species (analyses of synaptic densities in infants and adults of different species shows different patterns of development) (Byrnes & Fox, 1998). This all means we must be very careful when extrapolating from animal studies to possible implications for human learning.
Indeed, a report by the OECD goes on to make clear that there is no evidence in humans linking synaptic densities and improved learning, and there is no evidence relating synaptic densities in early life with those in later life. The reasoning has also been criticised on the grounds that the so-called ‘enriched’ environment for the rats was, in fact, much closer to a normal rat environment, so what the study showed was the detrimental effects of an artificially ‘deprived’ environment.
There is some human evidence to support the idea that loving environments have an effect on development. This derives from studies of Romanian orphans raised in severely impoverished environments (O'Connor et al, 1999). These children suffered ill effects from this privation although rehabilitation was still found to be possible if it occurred before six months of age.
To extrapolate from these findings, however, to the idea that young children should be brought up in an enriched environment to enhance their learning potential, is a bit farfetched. “Enriched”, when applied to early education for humans, is very much in the eye of the beholder, often reflecting the beholder’s cultural and class values’ (Bruer, 1997), and this preference is definitely not supported by neuroscience. What a baby needs is not an enriched academic environment but close contact with a primary caregiver, e.g., cuddling, eye contact, reciprocal communication, attention, security and love.
Thus, although research on synaptogenesis has the potential to be applied to learning strategies at the moment, the research on rats has been used pretentiously to encourage parents and other educationalists to buy into programmes that facilitate better learning. This is an example of how research findings can often be misapplied or used almost fraudulently to make money out of people.
“The idea of playing a game to make you sharper seems like a no-brainer. That is the thinking behind a billion-dollar industry selling brain training games and programs designed to boost cognitive ability. However, an investigation by CBC's Marketplace reveals that brain training games such as Lumosity may not make your brain perform better in everyday life. Zachary Hambrick, professor of cognitive neuroscience at Michigan State University, says “Companies need to demonstrate that playing the games make you better at doing everyday tasks, not just better at the games themselves.”
FUNCTIONAL RECOVERY OF THE BRAIN AFTER TRAUMA
FUNCTIONAL PLASTICITY:
Functional plasticity (also known as Adaptive plasticity): Functional plasticity allows our brain to adapt to injury, e.g., it refers to the brain’s ability to move functions from a damaged area of the brain to non-damaged areas (often in the other hemisphere or adjacent areas of the damaged area. Through sprouting of dendrites and re-routing of neurons.
INTRODUCTION:
“For many decades, it was thought that the brain was a nonrenewable organ,” that brain cells are bestowed in a finite amount and they slowly die as we age, whether we attempt to keep them around or not. “in adult centers, the nerve paths are something fixed, ended, immutable. Everything may die, nothing may be regenerated”
— Ramón y Cajal as cited in Fuchs & Flügge, 2014
Functional plasticity allows the brain to adapt to injury, e.g., it refers to the brain’s ability to move functions from a damaged area of the brain to non-damaged areas (often in the other hemisphere or adjacent areas of the damaged brain - through sprouting of dendrites, mirror neurons, the re-routing of neurons, and unmasking of non-recruited neurons).
.In the 1960s, researchers studied cases where stroke victims could regain functioning. They discovered that when brain cells are damaged or destroyed, as they are during a stroke, the brain re-wires itself over time so that some level of function can be regained. Although parts of the brain may be damaged or even destroyed because of trauma, other parts appear to take over the functions that were lost. Neurons next to the damaged brain areas can form new circuits that resume some of the lost function.
Stroke victims =individual differences.A03: Moreover, in the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60–80% of amputees. Explanations for this are based on the concept of neuroplasticity, as the cortical maps of the removed limbs are thought to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb. This is another example of functional recovery of the brain after trauma.
Mechanisms for recovery
Neural unmasking: What happens in the brain during recovery? The brain can rewire and reorganise itself by forming new synaptic connections close to the area of damage. Secondary neural pathways that would not typically be used to carry out certain functions are ‘unmasked’ to enable functioning to continue. Several structural changes support this process.
Axon sprouting: new nerve endings grow and connect with undamaged areas.
Stem cells.
Reformation of blood vessels.
Recruitment of homologous (similar) areas on the opposite hemisphere to do specific tasks - e.g. if Broca’s area was damaged then an area on the right might take over.
Neuronal Unmasking
Wall (1977) first identified what he called ‘dormant synapses’ in the brain. In short, dormant synapses’ are synaptic connections that exist anatomically, but their function is blocked. Under normal conditions, these synapses may be ineffective because the rate of neural input to them is too low for them to be activated. However, increasing the rate of input to these synapses, as would happen when a surrounding brain area becomes damaged, can then open (or ‘unmask’) these dormant synapses. The unmasking of dormant synapses can open connections to brain regions that are not normally activated, creating a lateral spread of activation which, in time, gives way to the development of new structures.
Human echolocation is an example of how brain damage can be rerouted. Human echolocation is the ability of humans to detect objects in their environment by sensing echoes from those objects by actively creating sounds – for example, by tapping their canes, lightly stomping their feet, snapping their fingers, or making clicking noises with their mouths. Studies in 2010 and 2011 using functional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. The results reveal that the echoes heard by these patients were processed by brain regions devoted to vision rather than audition.
In humans, evidence is restricted to small-scale studies of people who already have issues, it is unclear whether what we are seeing is due to recovery or an individual difference.
Stem cells are unspecialised cells that have the potential to give rise to different cell types that carry out different functions, including taking on the characteristics of nerve cells. There are several views on how stem cells might work to provide treatments for brain damage caused by injury or neurodegenerative disorders. The first view is that stem cells implanted into the brain would directly replace dead or dying cells. A second possibility is that transplanted stem cells secrete growth factors that somehow ‘rescue’ the injured cells. A third possibility is that transplanted cells from a neural network link an uninjured brain site, where new stem cells are made, with the damaged region of the brain.
This is supported by Tajiri et al (2013) provided evidence for the role of stem cells in recovery from brain injury. They randomly assigned rats with traumatic brain injury to one of 2 groups. One group received transplants of stem cells into the region of the brain affected by traumatic injury. The control group received a solution infused into the brain containing no stem cells. Three months after the brain injury, the brains of stem cell rats showed clear development of neuron-like cells in the area of injury. This was accompanied by a solid stream of stem cells migrating to the brain’s injury site. This was not the case with the control group.
There are also several factors to consider before saying that functional recovery is possible:
Age differences in functional recovery It is a commonly accepted view that functional plasticity reduces with age (Huttenlocher, 2002). According to this view, the only option following traumatic brain injury beyond childhood is to develop compensatory behavioural strategies to work around the deficit (such as seeking social support or developing strategies to deal with cognitive deficits). However, studies have suggested that even abilities commonly thought to be fixed in childhood can still be modified in adults with intense retraining.
Despite these indications of adult plasticity, Elbert et al (2001) conclude that the capacity for neural reorganisation is much greater in children than in adults, as demonstrated by the extended practice that adults require to produce changes. There are factors, however, that can make functional recovery more likely.
BENEFITS OF NEUROPLASTICITY ON THE BRAIN
Recovery from brain events like strokes
Recovery from traumatic brain injuries
Ability to rewire functions in the brain (e.g., if an area that controls one sense is damaged, other areas may be able to pick up the slack)
Losing function in one area may enhance functions in other areas (e.g. if one sense is lost, the others may become heightened.
Positive Plasticity
BRAIN FITNESS PROGRAM:
A structured set of brain exercises, usually computer-based, is designed to train specific brain areas and processes in targeted ways.
Educational attainment and functional recovery: Schneider et al (2014) found that patients with the equivalent of a college education are seven times more likely than those who didn’t finish high school to be disability-free one year after a moderate to severe traumatic brain injury. They carried out a retrospective study based on data from the US Traumatic Brain Injury Systems Database. Of the 769 patients studied, 214 had achieved disability-free recovery (DFR) after one year. Of these, 39.2% of the patients with 16 or more years of education had achieved DFR, as had 30.8% of those with 12-15 years of education, and just 9.7% of those with less than 12 years of education achieved DFR after just one year. The researchers concluded that ‘cognitive reserve’ (associated with greater educational attainment) could be a factor in neural adaptation during recovery from traumatic brain injury.
If the area is too damaged it is hard for the remaining areas to bridge the major tissue loss.
NEGATIVE PLASTICITY:
Plasticity does, however, have its downsides. Just as humans can develop plasticity to learn new skills, they can also develop it to ingrain a bad habit or a negative emotion. Neuroscientists separate neuroplasticity into types that have positive or negative behavioural consequences. For example, if an organism can recover after a stroke to normal levels of performance, that plasticity could be considered an example of "positive plasticity". Examples of negative plasticity include post-traumatic stress disorder, chronic pain disorders, phantom pain, changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury that could kill nerve cells or anything else in which neuronal communicating pathways have become more efficient at creating negative responses.
CHRONIC STRESS:
Ongoing, long-term stress blocks the formation of new neurons and negatively impacts the immune system’s defences.
COGNITIVE TRAINING:
Brain Fitness Training): the field of brain exercises designed to help work out specific “mental muscles. The principle underlying cognitive training is to help improve “core” abilities, such as attention, memory, processing speed, and problem-solving.
COGNITIVE RESERVE (OR BRAIN RESERVE):
The theory addresses the fact that individuals vary considerably in the severity of cognitive ageing and clinical dementia. Mental stimulation, education and occupational level are believed to be major active components of building a cognitive reserve that can help resist the attacks of mental disease
Negative plasticity: video games
A controversial example of negative plasticity can occur with children who frequently play violent, action, and video games. As these games are designed to be stress-provoking it makes sense that the children who play them might develop a reduction in their empathy or a less attuned stress response. This type of activity can cause negative plasticity in the brain’s survival-oriented limbic system.
Negative plasticity: teen addiction
New research suggests there may be a double-edged sword to the remarkably plastic and (thus very adaptive) teenage brain. Although the dramatic remodelling of the brain during adolescence holds tremendous opportunities for growth and learning it also appears to increase a teen’s vulnerability to the long-term effects of environmental influences such as stress and drug experimentation
Negative plasticity: teen addiction
One constant finding has been that adolescents are exceptionally vulnerable to drug addiction. This matches with the idea that addiction is a form of “over-learning”—because the adolescent brain is still quickly remodelling its circuits and learns faster (this essentially meaning the teen brain is very plastic). As a result, the teen brain may become addicted more deeply because the behaviours are, not only over learned; they almost become hardwired into the brain.
To test their hypothesis, the researchers gave adolescent and adult rats repeated access to cocaine in a particular environmental setting, essentially training the animals to associate that setting with the drug. After each drug exposure, the animals were freely allowed to return to the drug-associated environment or go to another area. Overall, adolescent rats showed a stronger preference for returning to the area associated with drug use.
A03: Extrapolating to human issues. Humans can choose not to start taking drugs.
WHY ARE HUMAN BRAINS SO PLASTIC: EVOLUTION?
The third theory suggests that humans are born with blank brains as it enables the nervous system to escape the restrictions of its genome and to become adaptive to all the environments and situations that humans might encounter, say from living in the Arctic and eating mainly meat, to living in the desert and being vegetarian for example. Other animals have less need for such plasticity as they have evolved to only thrive in one type of environment. A rhino fo example, can’t thrive anywhere but in a hot arid environment, because its brain is fixed at birth, it can’t learn new stuff. But a human can live and adapt to any climate, language or way of life.
“How to Rewire Your Brain with Neuroplasticity
Intermittent fasting increases synaptic adaptation, promotes neuron growth, improve overall cognitive function, and decreases the risk of neurodegenerative disease;
Travelling: exposes your brain to novel stimuli and new environments, opening up new pathways and activity in the brain;
Using mnemonic devices: memory training can enhance connectivity in the prefrontal parietal network and prevent some age-related memory loss;
Learning a musical instrument: may increase connectivity between brain regions and help form new neural networks;
Non-dominant hand exercises: can form new neural pathways and strengthen the connectivity between neurons;
Reading fiction: increases and enhances connectivity in the brain;
Expanding your vocabulary: activates the visual and auditory processes as well as memory processing;
Creating artwork: enhances the connectivity of the brain at rest (the “default mode network” or DMN), which can boost introspection, memory, empathy, attention, and focus (see art therapy activities);
Dancing: reduces the risk of Alzheimer’s and increases neural connectivity;
Sleeping: encourages learning retention through the growth of the dendritic spines that act as connections between neurons and help transfer information across cells”
Preventing Alzheimer’s And Cognitive Decline.
When an individual acquires an ability – for example, the ability to read – they actually create a system in the brain that does not exist, or that is not in place, in the non-reader. It [the ability] actually evolves in the brain. This is because the brain is designed and constructed to be stimulated and challenged and to carefully examine, resolve and interpret the environment. During the early days of humankind’s development, keeping track of the details was imperative for survival. Today, however, individuals remove themselves from the details of life. For example, instead of keeping track of appointments and to-do lists in their heads, they use electronic gadgets with reminder features. Roads and streets are paved and lit, requiring virtually no attention to navigate from one location to another. The theory surrounding cognitive decline is that if an individual does not sufficiently challenge their brain with new, surprising information, it will eventually begin to deteriorate. Cognitive Decline can be prevented by challenging the brain: reading, learning a language, meditation, etc.
"Generally, by the third or fourth decade of life, you're in decline. One of the things that happen across this period is that you go from a period of the acquisition of abilities to largely using those abilities that have been acquired earlier in life. By that, I mean to say, the fundamental skills that you apply in your profession or in your everyday life are things you master, and you are doing them without thought.
To a large extent, you are operating most of your day without really being consciously engaged in the things you are doing... I have gone without really thinking very much about the physical acts of driving. I am substantially disengaged.
This has been contributed substantially by modern culture. Modern culture is all about taking out surprises... to reduce the stimulation in a sense on one level so that we could engage ourselves in sort of an abstract level of operations. We are no longer interested in the details of things. We're no longer interested in resolving the details of what we see or hear or feel, and our brains slowly deteriorate." Dr. Merzenich
