- MIT scientists discover fundamental rule of brain plasticity
- Synaptic Plasticity: How It Works And Why It’s So Important
- What is Synaptic Plasticity?
- What is a Synapse?
- Glutamatergic System and Synaptic plasticity
- 1) Synaptic Plasticity is Important for Learning and Memory
- The Role of Synaptic Plasticity in The Hippocampus (Memory Center)
- 2) Synaptic Plasticity Helps Recover from Brain and Nervous System Injuries
- Conditions that Impair Synaptic Plasticity
- 2) Alzheimer’s and Parkinson’s Disease
- 3) PTSD
- 4) Schizophrenia, Anxiety, and Depression
- 5) Autism
- 6) Sleep Deprivation
- 7) Seizures
- 8) Other Diseases that May Involve Impaired Synaptic Plasticity
- 1) Brain-Derived Neurotrophic Factor (BDNF)
- 2) Healthy Glutamate Levels and Metabolism
- 3) Nerve Growth Factor (NGF)
- 4) Testosterone
- 5) Estradiol
- 6) Leptin
- 7) Secretin
- 8) Erythropoietin (EPO)
- 9) Pregnenolone Sulfate
- Further Reading
- Brain Plasticity & Early Intervention: “Neurons that fire together, wire together”
- What is brain plasticity and why is it so important?
- Growing then pruning
- Forging new paths
- Neuroscience for Kids – Brain Plasticity
- Facts About Neuroplasticity
- Developmental Plasticity: Synaptic Pruning
- Plasticity of Learning and Memory
- Injury-induced Plasticity: Plasticity and Brain Repair
MIT scientists discover fundamental rule of brain plasticity
Our brains are famously flexible, or “plastic,” because neurons can do new things by forging new or stronger connections with other neurons. But if some connections strengthen, neuroscientists have reasoned, neurons must compensate lest they become overwhelmed with input.
In a new study in Science, researchers at the Picower Institute for Learning and Memory at MIT demonstrate for the first time how this balance is struck: when one connection, called a synapse, strengthens, immediately neighboring synapses weaken the action of a crucial protein called Arc.
Senior author Mriganka Sur said he was excited but not surprised that his team discovered a simple, fundamental rule at the core of such a complex system as the brain, where 100 billion neurons each have thousands of ever-changing synapses. He ns it to how a massive school of fish can suddenly change direction, en masse, so long as the lead fish turns and every other fish obeys the simple rule of following the fish right in front of it.
“Collective behaviors of complex systems always have simple rules,” says Sur, the Paul E. and Lilah Newton Professor of Neuroscience in the Picower Institute and the Department of Brain and Cognitive Sciences at MIT. “When one synapse goes up, within 50 micrometers there is a decrease in the strength of other synapses using a well-defined molecular mechanism.”
This finding, he said, provides an explanation of how synaptic strengthening and weakening combine in neurons to produce plasticity.
Though the rule they found was simple, the experiments that revealed it were not. As they worked to activate plasticity in the visual cortex of mice and then track how synapses changed to make that happen, lead authors Sami El-Boustani and Jacque Pak Kan Ip, postdocs in Sur’s lab, accomplished several firsts.
In one key experiment, they invoked plasticity by changing a neuron’s “receptive field,” or the patch of the visual field it responds to. Neurons receive input through synapses on little spines of their branch- dendrites.
To change a neuron’s receptive field, the scientists pinpointed the exact spine on the relevant dendrite of the neuron, and then closely monitored changes in its synapses as they showed the mouse a target in a particular place on a screen that differed from the neuron’s original receptive field. Whenever the target was in the new receptive field position they wanted to induce, they reinforced the neuron’s response by flashing a blue light inside the mouse’s visual cortex, instigating extra activity just another neuron might. The neuron had been genetically engineered to be activated by light flashes, a technique called “optogenetics.”
The researchers did this over and over. Because the light stimulation correlated with each appearance of the target in the new position in the mouse’s vision, this caused the neuron to strengthen a particular synapse on the spine, encoding the new receptive field.
“I think it’s quite amazing that we are able to reprogram single neurons in the intact brain and witness in the living tissue the diversity of molecular mechanisms that allows these cells to integrate new functions through synaptic plasticity,” El-Boustani says.
As the synapse for the new receptive field grew, the researchers could see under the two-photon microscope that nearby synapses also shrank. They did not observe these changes in experimental control neurons that lacked the optogenetic stimulation.
But then they went further to confirm their findings. Because synapses are so tiny, they are near the limit of the resolution of light microscopy.
So after the experiments the team dissected the brain tissues containing the dendrites of manipulated and control neurons and shipped them to co-authors at the Ecole Polytechnique Federal de Lausanne in Switzerland.
They performed a specialized, higher-resolution, 3-D electron microscope imaging, confirming that the structural differences seen under the two-photon microscope were valid.
“This is the longest length of dendrite ever reconstructed after being imaged in vivo,” said Sur, who also directs the Simons Center for the Social Brain at MIT.
Of course, reprogramming a mouse’s genetically engineered neuron with flashes of light is an unnatural manipulation, so the team did another more classic “monocular deprivation” experiment in which they temporarily closed one eye of a mouse.
When that happens synapses in neurons related to the closed eye weaken and synapses related to the still open eye strengthen. Then when they reopened the previously closed eye, the synapses rearrange again.
They tracked that action, too, and saw that as synapses strengthen, their immediate neighbors would weaken to compensate.
Solving the mystery of the Arc
Having seen the new rule in effect, the researchers were still eager to understand how neurons obey it. They used a chemical tag to watch how key “AMPA” receptors changed in the synapses and saw that synaptic enlargement and strengthening correlated with more AMPA receptor expression while shrinking and weakening correlated with less AMPA receptor expression.
The protein Arc regulates AMPA receptor expression, so the team realized they had to track Arc to fully understand what was going on.
The problem, Sur said, is that no one had ever done that before in the brain of a live, behaving animal.
So the team reached out to co-authors at the Kyoto University Graduate School of Medicine and the University of Tokyo, who invented a chemical tag that could do so.
Using the tag, the team could see that the strengthening synapses were surrounded with weakened synapses that had enriched Arc expression. Synapses with reduced amount of Arc were able to express more AMPA receptors whereas increased Arc in neighboring spines caused those synapses to express less AMPA receptors.
“We think Arc maintains a balance of synaptic resources,” Ip says. “If something goes up, something must go down. That’s the major role of Arc.”
Sur says the study therefore solves a mystery of Arc: No one before had understood why Arc seemed to be upregulated in dendrites undergoing synaptic plasticity, even though it acts to weaken synapses, but now the answer was clear. Strengthening synapses increase Arc to weaken their neighbors.
Sur added that the rule helps explain how learning and memory might work at the individual neuron level because it shows how a neuron adjusts to the repeated simulation of another.
Ania Majewska, associate professor of neuroscience in the Center for Visual Science at the University of Rochester, says the study’s advanced methods allowed the team to achieve and important set of new results.
“Because of the difficulty in monitoring and manipulating the tiny and numerous synapses that connect neurons, most studies have been carried out in reduced preparations with artificial stimuli making it unclear how the mechanisms identified are actually implemented in the complicated circuits that function inside a brain reacting to its environment,” Majewska says. “This new study from the Sur lab has great impact because it combines cutting edge imaging and genetic tools to beautifully monitor the function of individual synapses inside a brain that is responding to behaviorally-relevant stimuli that elicit changes in neuronal responses.
“Given the results from this tour de force approach, we can now say that, in the intact brain, synapses that lie in close proximity to one another interact during changes in circuit function through a mechanism that involves a molecular cascade in which arc plays a critical role,” she said. “This information allows us to understand not only how neuronal circuits develop and remodel in a physiological setting, but provides clues that will be important in identifying how these processes go awry in various neurological diseases.”
In addition to Sur, El-Boustani and Ip, the paper’s other authors are Vincent Breton-Provencher, Ghraham Knott, Hiroyuki Okuno and Haruhiko Bito.
Funding for the research came from the Picower Institute Innovation Fund, The Simons Center for the Social Brain, a Marie Curie Postdoctoral Fellowship, a Human Frontier Science Program Long-Term Fellowship, the National Institutes of Health, the National Science Foundation, and KAKENHI.
Synaptic Plasticity: How It Works And Why It’s So Important
“Synaptic plasticity” refers to the process that the brain uses to adjust how neurons connect to each other and process information.
This process is extremely important for all forms of learning and memory, since the only way the brain can store new information is to change its own structure! Plasticity is also extremely important to the brain’s ability to recover from stress or damage, and is currently believed to play a major role in many different neurological and psychiatric disorders. Read on to learn more about plasticity, how it works, and why it’s so important!
What is Synaptic Plasticity?
It was once believed that the brain is extremely fragile, and that any damage to it is more or less permanent. This would mean that if a person’s brain was damaged or failed to develop properly in the first place, they were fated to live with it permanently!
However, the discovery of synaptic plasticity in 1966 overturned that belief. This gave new hope to people with brain damage, neurological diseases, or learning disabilities .
In fact, the brain is a lot more flexible and resilient than we previously thought! Neurons can re-grow and new neuronal connections can be made. This actually allows us to learn new skills and memories in everyday life since the brain is a physical organ, and therefore, has to change its structure in order to store any new information.
Synaptic plasticity is our brain’s key to the formation of new memories and neural networks – especially within the hippocampus, a brain structure that is believed to be heavily involved in memory.
Furthermore, neural plasticity may also be involved in repairing the brain from damage, such as from head traumas, stress, toxins, or even a lifetime of poor diet and lifestyle choices.
What is a Synapse?
Scientists currently estimate that our brain contains approximately 100 billion neurons. These neurons communicate with one another by forming synapses, which is the place where two neurons meet and connect.
However, this connection doesn’t involve direct physical contact, as it would on a circuit board, for example. Instead, each “synapse” is actually a tiny gap in between where the two neurons meet. This is where one neuron releases chemicals (neurotransmitters) in order to trigger an electrical response in the neighboring neuron.
By connecting into a series of synapses, this is how individual brain cells form signaling pathways, or “circuits”, which allows them to pass along and process information.
Synaptic plasticity refers to our brain’s ability to adjust the connections between neurons, which changes how they communicate with each other and process information. This process can be accomplished either by creating an entirely new synapse, or by adjusting the “strength” of an existing synapse .
When an existing synaptic connection is strengthened, this is called long-term potentiation (LTP). Conversely, when a connection is made weaker, this is called long-term depression (LTD).
Technically, “synaptic plasticity” refers only to changes that occur in the connections between neurons. However, you might also hear the term “neuronal plasticity,” which is a broader concept that includes synaptic plasticity as well as other biological changes to the brain, such as the creation of entirely new neurons (a process called neurogenesis).
Each of these processes is critical for a person’s ability to learn and store new information of all kinds! In other words, whether we’re talking about learning new motor skills (such as learning how to ride a bike) or if we’re talking about learning a new fact or forming a new memory, all of these abilities depend on the brain’s ability to adjust the way its cells connect to each other and process information.
Glutamatergic System and Synaptic plasticity
Glutamate is believed to be one of the most important neurotransmitters involved in synaptic plasticity .
Glutamate receptors that are involved include “AMPA” (hydroxy-3-methyl-4-isoxazole propionic acid) and “NMDA” (N-methyl d-aspartate) receptors.
Therefore, glutamate plays a key role in learning and memory.
Because glutamate is an excitatory neurotransmitter, it may be specifically related to long-term potentiation (LTP), which is the part of synaptic plasticity that refers to the strengthening of existing neural connections.
However, glutamate is far from the only critical factor! For example, many of the other major neurotransmitters – such as acetylcholine and other choline-based neurotransmitters – are also believed to be important for synaptic plasticity. There are also many other critical factors beyond just neurotransmitters, such as growth factors (“trophic factors”), which stimulate the brain into creating new neurons and synapses .
1) Synaptic Plasticity is Important for Learning and Memory
Intrinsic brain plasticity, or the brain’s inherent ability to rewire itself, is an important and evolutionarily conserved neural correlate of all forms of learning .
Intrinsic plasticity is also an important predictor of learning-induced behavioral plasticity .
Synaptic plasticity allows for long-term potentiation – or increasing the strength of our synapses with more use, which allows us to memorize or become fluent at the things we learn. Therefore, synaptic plasticity is essential for learning and memory .
The Role of Synaptic Plasticity in The Hippocampus (Memory Center)
Located in the medial temporal lobe, the hippocampus plays a key role in forming new associations and consolidating stimuli into new memories .
Specialized cells in the hippocampus can also undergo cell division (mitosis) to generate entirely new brain cells (neurogenesis) . Synaptic plasticity is important for these cells to integrate with other hippocampal cells.
2) Synaptic Plasticity Helps Recover from Brain and Nervous System Injuries
Neuroplasticity is what allows the central nervous system to (partially) recover from damage, such as brain injuries. In addition, the brain can adapt through secondary compensatory mechanisms when there is some brain tissue damage .
Some preliminary research suggests that long-lasting morphological changes occur in the hippocampus after traumatic brain injury – including the growth of cell bodies (soma) and recruitment of new neurons into the hippocampus [11, 12].
Spinal injuries that damage the sensorimotor pathways are known to cause synaptic changes in neuronal circuitry, within the spinal cord and at higher levels, over the postinjury weeks and months .
Conditions that Impair Synaptic Plasticity
Cognitive function naturally declines with age. At least part of this age-related cognitive decline is believed to be due to a gradual loss of plasticity throughout the brain – and especially in certain key memory-related areas, such as the hippocampus .
2) Alzheimer’s and Parkinson’s Disease
Alzheimer’s and Parkinson’s diseases are believed to be caused by the build-up of beta-amyloid “plaques” in the neurons of the brain.
While this build-up can lead to cell death due to toxicity, there is some evidence that it may also interfere with processes related to synaptic plasticity – in other words, these amyloid plaques may interfere with brain processes even without outright killing the brain cells themselves [15, 16].
Some preliminary research suggests that synaptic plasticity in the amygdala may be involved in PTSD, and has been proposed to be an important target for its treatment .
4) Schizophrenia, Anxiety, and Depression
According to some researchers, synaptic plasticity may also have a role in the development of anxiety and schizophrenia .
More specifically, some scientists have proposed that schizophrenia may be a disease of short-term synaptic plasticity alterations .
According to some studies, AMPA receptors are inhibited in schizophrenia patients. This may interfere with long-term potentiation, and thus impair one’s ability to form new memories .
Interestingly, depression also appears to involve impairments in synaptic plasticity – and some evidence suggests that the actions of common antidepressant medications (such as SSRIs and other monoamine-targeting drugs) may alleviate depression by increasing or restoring synaptic plasticity throughout the brain [21, 22].
Some early evidence suggests that autism may involve disruptions in multiple signaling pathways that are activated during synaptic plasticity, which may suggest that impaired synaptic plasticity could be one of the main causes or consequences of autism-spectrum disorders [23, 24, 25].
6) Sleep Deprivation
Getting enough high-quality sleep is critical for stimulating synaptic plasticity.
By extension, sleep deprivation can significantly interfere with synaptic plasticity.
For example, according to one study, just 5–6 hours of sleep deprivation is sufficient to impair long-term potentiation, thus potentially hindering synaptic plasticity in general .
Another study has suggested that stressful events early in life may induce long-term sleep disturbances, which could, in turn, alter or impair synaptic plasticity in the long term .
According to some early research, rats with seizures show alterations in the long-term potentiation within synapses throughout the somatosensory cortex .
8) Other Diseases that May Involve Impaired Synaptic Plasticity
- Borna disease virus infection has been reported to impair synaptic plasticity 
- Angelman syndrome has been reported to impair synaptic plasticity (due to cell mutations) [20, 29]
- Noonan syndrome 
- Tuberous sclerosis 
1) Brain-Derived Neurotrophic Factor (BDNF)
Brain‐derived neurotrophic factor (BDNF) is well-known for supporting neuronal survival and growth throughout the brain, and plays an especially important role in synaptic plasticity in the hippocampus, in particular .
2) Healthy Glutamate Levels and Metabolism
Glutamate transport has been associated with the formation of new synapses, synaptic plasticity, as well as learning and memory at large [31, 32].
3) Nerve Growth Factor (NGF)
BDNF, nerve growth factor (NGF) is another major growth factor (neurotrophic factor) that supports synaptic plasticity and promotes long-term memory formation [33, 34].
According to some animal studies, testosterone may be associated with memory performance and synaptic plasticity in male rats [35, 36].
Estradiol (an estrogen signaling molecule) has been reported to affect hippocampal-dependent spatial memory and synaptic plasticity in female mice and rats [37, 38].
According to some animal studies, administration of the hormone leptin into the brain has been reported to help facilitate hippocampal long-term potentiation, and may even improve memory performance [39, 40].
Secretin has been linked to synaptic plasticity and social behavior in mice .
8) Erythropoietin (EPO)
In a rat model of Alzheimer’s, erythropoietin was reported to improve synaptic plasticity and reduce glutamate levels (which are typically elevated in Alzheimer’s) .
9) Pregnenolone Sulfate
Pregnenolone sulfate is a steroid hormone (neuromodulator) that has been reported to have some potential beneficial effects on the brain. By enhancing NMDA and other neurotransmitter receptors, pregnenolone seems to help with synaptic plasticity for learning and memory – although more research will be needed to explore these potential effects further .
Now that you’re all up to speed about how synaptic plasticity works and why it’s so important, you might be wondering if there are any possible ways to “boost” your own brain’s synaptic plasticity!
While there are no officially-approved treatments or other strategies to do this, there is some preliminary research that suggests that a wide variety of dietary compounds and supplements may have significant effects on overall synaptic plasticity.
To learn more about what these compounds are and what the latest science says about them, check out our follow-up post here.
Brain Plasticity & Early Intervention: “Neurons that fire together, wire together”
The following is a conversation Ronit Molko, Ph.D., BCBA-D and Dr. Evian Gordon, Chairman and CEO of Brain Resource.
The development of the brain is a fascinating and essential aspect of child development. The science behind the brain provides parents and practitioners valuable insight into why early intervention is so important for individuals with autism and other developmental disabilities.
At birth, a child’s brain is unfinished. It develops as they experience the world through seeing, hearing, tasting, touching and smelling the environment.
The natural, simple, loving encounters with adults that occur through the day, such as a caregiver singing, smiling, talking and rocking their baby, are essential to this process.
All of these encounters with the outside world affect the child’s emotional development and shape how their brain becomes wired and how it will work.
The experiences of babies have long-lasting effects on their ability to learn and regulate their emotions.
When there is an absence of appropriate teaching and learning opportunities in the baby’s environment, the brain’s development can be affected and there are more ly to be sustained negative effects.
Conversely, if we can provide ample learning opportunities, we can facilitate brain development. Let’s understand how and why.
Learning is about connection. A baby is born with more than 85 billion neurons in its brain.
Neurons are nerve cells in the brain that transmit information between each other through chemical and electrical signals via synapses thereby forming neural networks, a series of interconnected neurons. This is what is meant by “the wiring of the brain” and “neurons that fire together, wire together”.
As an infant experiences something or learns something for the first time, a strong neural connection is made. If this experience is repeated, the connection is reactivated and becomes strengthened. If the experience is not repeated, connections are removed.
In this way, the brain “prunes” what is not necessary and consolidates the connections that are necessary. During infancy and the first years of childhood, there is significant loss of neural pathways as the brain starts to prune away what it doesn’t believe it will need to function.
The earlier in a child’s development that we create that first, correct learning experience the stronger those behaviors and skills are secured in the brain.
Children with developmental delays often experience the wiring of neurons together in a manner that is “unhelpful”, causing them to struggle with communication, social skills and other activities. These “unhelpful” connections need to be changed, which adds to the challenge and takes time.
Technically, learning cannot be undone in the brain, but amazingly, with stimulation, the brain has the ability to re-process new pathways and build circuits that are helpful and functional. The brain has a remarkable capacity for change and adaptation, but timing is crucial.
The earlier we create the correct connections in a child’s brain, the stronger those behaviors and skills are secured in the brain.
Intervention is best during early childhood when there are 50 percent more connections between neurons than exist in the adult brain.
When a child reaches adolescence, another period of pruning begins where the brain starts to cut back on these important brain connections, and neurons that have not been used much.
For children with all types of learning difficulties and developmental disorders, this understanding of the brain’s plasticity is particularly relevant, because it emphasizes why the correct type and intensity of early intervention is so critical.
If we correctly understand a child’s skill deficits and design a program that appropriately stimulates the neurons in the targeted weakened areas of the brain, we can exercise and strengthen those areas of the brain to develop language, social skills etc.
So how do you train your child’s brain? In order to change the brain’s wiring and make new neural connections, a new skill needs to be practiced many times so Dr. Gordon recommends starting with one, simple task and practicing it at least 10 times per day. Measure how long it takes for your child’s behavior to change. This will help you determine your child’s rate of learning.
An example of a simple task would be teaching your child to follow a simple instruction using a preferred item such as asking him to eat his favorite food.
You can then move onto a more complex activity such as requesting eye contact by saying “Look at me” and then something more complex such as “touch the car” when playing with a toy car, for example.
There are many opportunities throughout the day during normal daily parenting activities (bathing, feeding, diapering, reading, etc.) during which you can support your child’s development and train his brain to respond to people and his environment.
One common question is what is possible with the brain after childhood? For many years, science has told us that brain plasticity is at its peak during childhood.
However, experts now believe that under the correct circumstances, practicing a new skill can change hundreds of millions, if not billions, of connections between nerve cells in the brain even into adulthood. It is never too late to start.
The most important thing to remember is that learning is what changes the brain and learning takes practice. Every opportunity to teach your child is an opportunity to shape their brain and change their future.
For more information, visit Developmental Milestones from the Child Mind Institute http://www.childmind.org/en/developmental-milestones/
Learn more about the work and resources of Dr. Evian Gordon at
Harvard’s “Serve & Retrun” concept of parent engagement
What is brain plasticity and why is it so important?
Neuroplasticity – or brain plasticity – is the ability of the brain to modify its connections or re-wire itself. Without this ability, any brain, not just the human brain, would be unable to develop from infancy through to adulthood or recover from brain injury.
What makes the brain special is that, un a computer, it processes sensory and motor signals in parallel. It has many neural pathways that can replicate another’s function so that small errors in development or temporary loss of function through damage can be easily corrected by rerouting signals along a different pathway.
The problem becomes severe when errors in development are large, such as the effects of the Zika virus on brain development in the womb, or as a result of damage from a blow to the head or following a stroke. Yet, even in these examples, given the right conditions the brain can overcome adversity so that some function is recovered.
The brain’s anatomy ensures that certain areas of the brain have certain functions. This is something that is predetermined by your genes. For example, there is an area of the brain that is devoted to movement of the right arm. Damage to this part of the brain will impair movement of the right arm.
But since a different part of the brain processes sensation from the arm, you can feel the arm but can’t move it. This “modular” arrangement means that a region of the brain unrelated to sensation or motor function is not able to take on a new role.
In other words, neuroplasticity is not synonymous with the brain being infinitely malleable.
Part of the body’s ability to recover following damage to the brain can be explained by the damaged area of the brain getting better, but most is the result of neuroplasticity – forming new neural connections.
In a study of Caenorhabditis elegans, a type of nematode used as a model organism in research, it was found that losing the sense of touch enhanced the sense of smell. This suggests that losing one sense rewires others.
It is well known that, in humans, losing one’s sight early in life can heighten other senses, especially hearing.
As in the developing infant, the key to developing new connections is environmental enrichment that relies on sensory (visual, auditory, tactile, smell) and motor stimuli.
The more sensory and motor stimulation a person receives, the more ly they will be to recover from brain trauma.
For example, some of the types of sensory stimulation used to treat stroke patients includes training in virtual environments, music therapy and mentally practising physical movements.
The basic structure of the brain is established before birth by your genes.
But its continued development relies heavily on a process called developmental plasticity, where developmental processes change neurons and synaptic connections.
In the immature brain this includes making or losing synapses, the migration of neurons through the developing brain or by the rerouting and sprouting of neurons.
There are very few places in the mature brain where new neurons are formed.
The exceptions are the dentate gyrus of the hippocampus (an area involved in memory and emotions) and the sub-ventricular zone of the lateral ventricle, where new neurons are generated and then migrate through to the olfactory bulb (an area involved in processing the sense of smell). Although the formation of new neurons in this way is not considered to be an example of neuroplasticity it might contribute to the way the brain recovers from damage.
Growing then pruning
As the brain grows, individual neurons mature, first by sending out multiple branches (axons, which transmit information from the neuron, and dendrites, which receive information) and then by increasing the number of synaptic contacts with specific connections.
Why doesn’t everyone make a full recovery after a stroke? www.shutterstock.com
At birth, each infant neuron in the cerebral cortex has about 2,500 synapses. By two or three-years-old, the number of synapses per neuron increases to about 15,000 as the infant explores its world and learns new skills – a process called synaptogenesis. But by adulthood the number of synapses halves, so-called synaptic pruning.
Whether the brain retains the ability to increase synaptogenesis is debatable, but it could explain why aggressive treatment after a stroke can appear to reverse the damage caused by the lack of blood supply to an area of the brain by reinforcing the function of undamaged connections.
Forging new paths
We continue to have the ability to learn new activities, skills or languages even into old age. This retained ability requires the brain to have a mechanism available to remember so that knowledge is retained over time for future recall. This is another example of neuroplasticity and is most ly to involve structural and biochemical changes at the level of the synapse.
Reinforcement or repetitive activities will eventually lead the adult brain to remember the new activity. By the same mechanism, the enriched and stimulating environment offered to the damaged brain will eventually lead to recovery.
So if the brain is so plastic, why doesn’t everyone who has a stroke recover full function? The answer is that it depends on your age (younger brains have a better chance of recovery), the size of the area damaged and, more importantly, the treatments offered during rehabilitation.
Neuroscience for Kids – Brain Plasticity
Long lasting functional changes in the brain occur when we learn new things or memorize new information. These changes in neural connections are what we call neuroplasticity.
To illustrate the concept of plasticity, imagine the film of acamera. Pretend that the film represents your brain.
Now imagine usingthe camera to take a picture of a tree. When a picture is taken, the filmis exposed to new information — that of the image of a tree. In orderfor the image to be retained, the film must react to the light and”change” to record the image of the tree.
Similarly, in order for newknowledge to be retained in memory, changes in the brain representing thenew knowledge must occur.
To illustrate plasticity in another way, imagine making an impressionof a coin in a lump of clay. In order for the impression of the coin toappear in the clay, changes must occur in the clay — the shape of theclay changes as the coin is pressed into the clay. Similarly, the neuralcircuitry in the brain must reorganize in response to experience orsensory stimulation.
Facts About Neuroplasticity
FACT 1: Neuroplasticity includes severaldifferent processes that take place throughout a lifetime.
Neuroplasticity does not consist of a single type ofmorphological change, but rather includes several different processes thatoccur throughout an individual's lifetime.
Many types of brain cells are involved in neuroplasticity, including neurons, glia, and vascularcells.
FACT 2: Neuroplasticity has a clear age-dependent determinant.
Although plasticity occurs over an individual's lifetime, different types ofplasticity dominate during certain periods of one's life and are lessprevalent during other periods.
FACT 3: Neuroplasticity occurs in the brain under two primary conditions:
1. During normal brain development when the immature brain firstbegins to process sensory information through adulthood (developmentalplasticity and plasticity of learning and memory).
2. As an adaptivemechanism to compensate for lost function and/or to maximize remainingfunctions in the event of brain injury.
FACT 4: The environment plays a key role in influencing plasticity.
In addition to genetic factors, the brain is shaped by thecharacteristics of a person's environment and by the actions of that sameperson.
Developmental Plasticity: Synaptic Pruning
Gopnick et al. (1999) describe neurons as growing telephone wires that communicate with one another. Following birth, the brain of a newborn is flooded with information from the baby's sense organs. This sensory information must somehow make it back to the brain where it can be processed.
To do so, nerve cells must make connections with one another, transmitting the impulses to the brain. Continuing with the telephone wire analogy, the basic telephone trunk lines strung between cities, the newborn's genes instruct the “pathway” to the correct area of the brain from a particular nerve cell.
For example, nerve cells in the retina of the eye send impulses to the primary visual area in the occipital lobe of the brain and not to the area of language production (Wernicke's area) in the left posterior temporal lobe.
The basic trunk lines have been established, but the specific connections from one house to another require additional signals.
Over the first few years of life, the brain grows rapidly.
As eachneuron matures, it sends out multiple branches (axons, which sendinformation out, and dendrites, which take in information), increasing thenumber of synaptic contacts and laying the specific connections fromhouse to house, or in the case of the brain, from neuron to neuron.
Atbirth, each neuron in the cerebral cortex has approximately 2,500 synapses. By the time an infant is two or threeyears old, the number of synapses is approximately 15,000 synapses perneuron (Gopnick, et al., 1999). This amount is about twice that of theaverage adult brain. As we age, old connections are deleted through aprocess called synaptic pruning.
Synaptic pruning eliminates weaker synaptic contacts while strongerconnections are kept and strengthened. Experience determines whichconnections will be strengthened and which will be pruned; connectionsthat have been activated most frequently are preserved. Neurons must havea purpose to survive.
Without a purpose, neurons die through a processcalled apoptosis in which neurons that do not receive or transmitinformation become damaged and die. Ineffective or weak connections are”pruned” in much the same way a gardener would prune a tree or bush,giving the plant the desired shape.
It is plasticity that enables theprocess of developing and pruning connections, allowing the brain to adaptitself to its environment.
Plasticity of Learning and Memory
It was once believed that as we aged, the brain's networks becamefixed. In the past two decades, however, an enormous amount of researchhas revealed that the brain never stops changing and adjusting.
Learning, as defined by Tortora and Grabowski (1996), is the abilityto acquire new knowledge or skills through instruction or experience. Memory is the process by which that knowledge is retained over time. Thecapacity of the brain to change with learning is plasticity.
So how doesthe brain change with learning? According to Durbach (2000), there appearto be at least two types of modifications that occur in the brain withlearning:
- A change in the internal structure of the neurons, the most notable being in the area of synapses.
- An increase in the number of synapses between neurons.
Initially, newly learned data are “stored” in short-term memory,which is a temporary ability to recall a few pieces of information.
Someevidence supports the concept that short-term memory depends uponelectrical and chemical events in the brain as opposed to structuralchanges such as the formation of new synapses.
One theory of short-termmemory states that memories may be caused by “reverberating” neuronalcircuits — that is, an incoming nerve impulse stimulates the first neuronwhich stimulates the second, and so on, with branches from the secondneuron synapsing with the first.
After a period of time, information maybe moved into a more permanent type of memory, long-term memory, which isthe result of anatomical or biochemical changes that occur in the brain(Tortora and Grabowski, 1996).
Injury-induced Plasticity: Plasticity and Brain Repair
During brain repair following injury, plastic changes are gearedtowards maximizing function in spite of the damaged brain. In studiesinvolving rats in which one area of the brain was damaged, brain cellssurrounding the damaged area underwent changes in their function andshape that allowed them to take on the functions of the damagedcells. Although this phenomenon has not been widely studied in humans,data indicate that similar (though less effective) changes occur in humanbrains following injury.