What is neuroplasticity?
Brain damage
Due to more recent Medical, Rehabilitation and ongoing results 'neuroplasticity' within the mechanics of our brains lead to re-arrangement of the brain's workings. These often result in the synapses arranging alternate routes, to achieve previous habits. Neuroplasticity is the brain's ability to reorganise itself by forming new neural connections throughout life. Neuroplasticity allows the neurons (nerve cells) in the brain to compensate for injury and disease and to adjust their activities in response to new situations or to changes in their environment.
Spike-timing-dependent plasticity
Spike-timing-dependent plasticity (STDP) is a biological process that adjusts the strength of connections between neurons in the brain. The process adjusts the connection strengths based on the relative timing of a particular neuron's output and input action potentials (or spikes). The STDP process partially explains the activity-dependent development of nervous systems, especially with regard to long-term potentiation and long-term depression.
Metaplasticity
A new mechanism has been proposed that concerns the innate excitability of a neuron. It is quantified by the size of the hyperpolarization in mV due to K+ channels re-opening during an action potential. After any sort of learning task, particularly a classical or operant conditioning task, the amplitude of the K+ hyperpolarization, or "after hyperpolarization (AHP)", is greatly reduced. Over time this AHP will return to normal levels. This normalization does not correlate with a loss of memory but instead a loss of learning potential.
Cortical map
Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". An excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury which could kill nerve cells; this would have to be considered a "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.
Neuroplastic surgery
Training in neuroplastic surgery requires completion of a neuroplastic and reconstructive surgery fellowship which lasts 1–2 years. Such fellowships are available to individuals who have completed a residency in Plastic and Reconstructive Surgery, ENT Surgery, Neurosurgery or Oral and Maxillofacial surgery. As of today, the only formal fellowship training program in neuroplastic and reconstructive surgery is located at the Johns Hopkins School of Medicine and Johns Hopkins Hospital. The fellowship is co-sponsored by both Departments of Plastic Surgery and Neurosurgery. The first surgeon formally trained in "Neuroplastic and Reconstructive Surgery" was Dr. Gabriel Santiago [2016-18], who completed ENT surgery residency in the US Navy prior to starting the fellowship. The first Neuroplastic Surgery Research Fellow was Dr. Amir Wolff [2017-18], an attending oral-maxillofacial surgeon from Rambam Medical Center in Haifa, Israel.
Cultured neuronal network
There is much controversy in the field of neuroscience surrounding whether or not a cultured neuronal network can learn. A crucial step in finding the answer to this problem lies in establishing the difference between learning and plasticity. One definition suggests that learning is "the acquisition of novel behavior through experience". Corollary to this argument is the necessity for interaction with the environment around it, something that cultured neurons are virtually incapable of without sensory systems. Plasticity, on the other hand, is simply the reshaping of an existing network by changing connections between neurons: formation and elimination of synapses or extension and retraction of neurites and dendritic spines. But these two definitions are not mutually exclusive; in order for learning to take place, plasticity must also take place.
Neuronal memory allocation
One aspect of integration involves metaplasticity and how acquisition and storage of one memory changes the neural circuit to affect the storage and properties of a subsequent memory. Cellular excitability has been proposed as one of the mechanisms responsible for heterosynaptic metaplasticity, the modulation of subsequent plasticity at different synapses. CREB functions through elevating cell excitability as described above, thus it is also possibly involved in hetrerosynaptic metaplasticity. Synaptic tagging and capture, as introduced in sections above, can result in a weak memory (capable of triggering only E-LTP), which would otherwise be forgotten, but it can be strengthened and stabilized by a strong memory (capable of triggering L-LTP), which is a form of heterosynaptic plasticity.
Enchroma
In some subjects, improvements due to the technology do not happen immediately because the brain requires time to rewire and create new links, neuroplasticity. Neuroplasticity depends on the age of the individual. Younger people reported that they perceived little changes from the first time they wore glasses and a second wearing in which they have had time to adapt to the technology. Middle age people reported that the colors continued to change from the first time they wore the lens, and that color brightness and enhancement got better with time. Most participants related that the biggest effects of the glasses are not perceived initially but after a few days, confirming that the neuroplasticity takes time.
Nervous system
One very important subset of synapses are capable of forming memory traces by means of long-lasting activity-dependent changes in synaptic strength. The best-known form of neural memory is a process called long-term potentiation (abbreviated LTP), which operates at synapses that use the neurotransmitter glutamate acting on a special type of receptor known as the NMDA receptor. The NMDA receptor has an "associative" property: if the two cells involved in the synapse are both activated at approximately the same time, a channel opens that permits calcium to flow into the target cell. The calcium entry initiates a second messenger cascade that ultimately leads to an increase in the number of glutamate receptors in the target cell, thereby increasing the effective strength of the synapse. This change in strength can last for weeks or longer. Since the discovery of LTP in 1973, many other types of synaptic memory traces have been found, involving increases or decreases in synaptic strength that are induced by varying conditions, and last for variable periods of time. The reward system, that reinforces desired behaviour for example, depends on a variant form of LTP that is conditioned on an extra input coming from a reward-signalling pathway that uses dopamine as neurotransmitter. All these forms of synaptic modifiability, taken collectively, give rise to neural plasticity, that is, to a capability for the nervous system to adapt itself to variations in the environment.
Cognitive development
During development, especially the first few years of life, children show interesting patterns of neural development and a high degree of neuroplasticity. Neuroplasticity, as explained by the World Health Organization, can be summed up in three points. 1.) Any adaptive mechanism used by the nervous system to repair itself after injury. 2.) Any means by which the nervous system can repair individually damaged central circuits. 3.) Any means by which the capacity of the central nervous system can adapt to new physiological conditions and environment. The relation of brain development and cognitive development is extremely complex and, since the 1990s, has been a growing area of research.
Developmental plasticity
While synaptic plasticity is considered to be a by-product of learning, learning requires interaction with the environment to acquire the new information or behavior, whereas synaptic plasticity merely represents the change in strength or configuration of neural circuits. Learning is of crucial importance postnatally as there is considerable interaction with the environment and the potential for acquiring new information is greatest. By depending largely upon selective experiences, neural connections are altered and strengthened in a manner that is unique to those experiences. Experimentally this can be seen when rats are raised in an environment that allows ample social interaction, resulting in increased brain weight and cortical thickness. In contrast, the adverse is seen following rearing in an environment devoid of interaction. Also, learning plays a sizeable role in the selective acquisition of information and is markedly demonstrated as children develop one language as opposed to another. Another example of such experience dependent plasticity that is critical during development is the occurrence of imprinting. This occurs as a result of the young child or animal experiencing a novel stimuli and rapidly learning the behavior in response.
Neuroplasticity
Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London's layout in local taxi drivers. A redistribution of grey matter was indicated in London Taxi Drivers compared to controls. This work on hippocampal plasticity not only interested scientists, but also engaged the public and media worldwide.
Neuroplasticity
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. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed 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.
Neurobiological effects of physical exercise
Neuroplasticity is the process by which neurons adapt to a disturbance over time, and most often occurs in response to repeated exposure to stimuli. Aerobic exercise increases the production of neurotrophic factors (e.g., BDNF, IGF-1, VEGF) which mediate improvements in cognitive functions and various forms of memory by promoting blood vessel formation in the brain, adult neurogenesis, and other forms of neuroplasticity. Consistent aerobic exercise over a period of several months induces clinically significant improvements in executive functions and increased gray matter volume in nearly all regions of the brain, with the most marked increases occurring in brain regions that give rise to executive functions. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex, caudate nucleus, and hippocampus; less significant increases in gray matter volume occur in the anterior cingulate cortex, parietal cortex, cerebellum, and nucleus accumbens. The prefrontal cortex, caudate nucleus, and anterior cingulate cortex are among the most significant brain structures in the dopamine and norepinephrine systems that give rise to cognitive control. Exercise-induced neurogenesis (i.e., the increases in gray matter volume) in the hippocampus is associated with measurable improvements in spatial memory. Higher physical fitness scores, as measured by VO max, are associated with better executive function, faster information processing speed, and greater gray matter volume of the hippocampus, caudate nucleus, and nucleus accumbens. Long-term aerobic exercise is also associated with persistent beneficial epigenetic changes that result in improved stress coping, improved cognitive function, and increased neuronal activity ( and BDNF signaling).
List of medical mnemonics
Neoplastic
Neuromorphology
Neuromorphology has been used as a new method of exploring the underlying cause of many neurological disorders, and has been included in the clinical study of various neurodegenerative diseases, mental disorders, learning disabilities, and dysfunctions due to brain damage. Researchers have been using neuromorphological techniques to not only study the damage but also ways to regenerate the damage nerve through ways like axon growth stimulation.
Neuromophology has been used to study optical nerve damage, specifically looking at lesions and atrophies. Researchers have also examined and identified the neuromorphology of the human penis to better understand the role the sympathetic nervous system plays in achieving an erection.
Colin Blakemore
Although initially controversial, the idea that the mammalian brain is 'plastic' and adaptive is now a dominant theme in neuroscience. The plasticity of connections between nerve cells is thought to underlie many different types of learning and memory, as well as sensory development. The changes in organisation can be remarkably rapid, even in adults. Blakemore has shown that the visual parts of the human cortex become responsive to input from the other senses, especially touch, in people who have been blind since shortly after birth. After stroke or other forms of brain injury, reorganisation of this sort can help the process of recovery, as other parts of the brain take over the function of the damaged part.
NPTN
Neuroplastin is a protein that in humans is encoded by the "NPTN" gene.
Paul Bach-y-Rita
The chair he used had a bank of four hundred vibrating plates resting against the blind user's back, and vibrating in connection with a camera placed above the chair, looking forwards. The pattern in which the stimulation occurred enabled the user to "see", often being able to recognise an object coming towards the camera. Bach-y-Rita suggested this was an example of neuroplasticity, as he believed the signals sent to the brain from the skin via touch were being processed in the visual cortex, because of the way the patients interpreted the information.
Heterosynaptic plasticity
A neural network that undergoes plastic changes between synapses must initiate normalization mechanisms in order to combat unrestrained potentiation or depression. One mechanism assures that the average firing rate of these neurons is kept at a reasonable rate through synaptic scaling. In this process, input levels are changed in cells to maintain average firing rate. For example, inhibitory synapses are strengthened or excitatory synapses are weakened to normalize the neural network and allow single neurons to regulate their firing rate.
Another mechanism is the cell-wide redistribution of synaptic weight. This mechanism conserves the total synaptic weight across the cell by introducing competition between synapses. Thus, normalizing a single neuron after plasticity. During development, cells can be refined when some synapses are preserved and others are discarded to normalize total synaptic weight. In this way, homeostasis is conserved in cells that are undergoing plasticity and normal operation of learning networks is also preserved, allowing new information to be learned.
Neuroplastic surgery
Neuroplastic surgery has adapted reconstructive principles from the fields of craniofacial surgery, and plastic and reconstructive surgery and refined them in order to address challenging deformities which result from Neurosurgical Procedures. The first center for Neuroplastic and Reconstructive Surgery was started at Johns Hopkins University Hospital in Baltimore, Maryland by a formal collaboration between the Department of Plastic and Reconstructive Surgery, under the guidance of plastic surgeon Chad Gordon, and the Department of Neurosurgery under the guidance of neurosurgeon Judy Huang. Upon arrival to Johns Hopkins Hospital, Dr. Chad Gordon formed a multi-disciplinary team of physicians, scientists and engineers. The team’s unified goal was to develop techniques and devices to treat neurosurgical patients. These advances led to several publications and patents, and allowed for the establishment of the first formal fellowship training program in Neuroplastic and Reconstructive Surgery. In March 2018, Dr. Gordon was appointed the Director of Neuroplastic and Reconstructive Surgery at Johns Hopkins.
Activity-dependent plasticity
Activity-dependent plasticity is a form of functional and structural neuroplasticity that arises from the use of cognitive functions and personal experience; hence, it is the biological basis for learning and the formation of new memories. Activity-dependent plasticity is a form of neuroplasticity that arises from intrinsic or endogenous activity, as opposed to forms of neuroplasticity that arise from extrinsic or exogenous factors, such as electrical brain stimulation- or drug-induced neuroplasticity. The brain's ability to remodel itself forms the basis of the brain's capacity to retain memories, improve motor function, and enhance comprehension and speech amongst other things. It is this trait to retain and form memories that is associated with neural plasticity and therefore many of the functions individuals perform on a daily basis. This plasticity occurs as a result of changes in gene expression which are triggered by signaling cascades that are activated by various signaling molecules (e.g., calcium, dopamine, and glutamate, among many others) during increased neuronal activity.
Neural backpropagation
Backpropagating action potentials can induce Long-term potentiation by behaving as a signal that informs the presynaptic cell that the postsynaptic cell has fired. Moreover, Spike-Time Dependent Plasticity is known as the narrow time frame for which coincidental firing of both the pre and post synaptic neurons will induce plasticity. Neural backpropagation occurs in this window to interact with NMDA receptors at the apical dendrites by assisting in the removal of voltage sensitive Mg2+ block (Waters et al., 2004). This process permits the large influx of calcium which provokes a cascade of events to cause potentiation.
Albrecht Bethe
He is well known for his studies involving the nervous system of invertebrates. He believed in the "plasticity" of the nervous system, asserting that if one part of the brain is damaged, another part could learn the functions of the damaged portion.
Neuroplasticity
The term has since seen broadly applied:
Synaptic scaling
Hebbian plasticity and homeostatic plasticity have a hand-in-glove relationship. Neurons use Hebbian plasticity mechanisms to modify their synaptic connections within the neural circuit based on the correlated input they receive from other neurons. Long-term potentiation (LTP) mechanisms are driven by related pre-synaptic and post-synaptic neuron firings; with the help of homeostatic plasticity, LTPs and LTDs create and maintain the precise synaptic weights in the neural network. Persisting correlated neural activity—without a homeostatic feedback loop—causes LTP mechanisms to continually up regulate synaptic connection strengths. Unspecified strengthening of synaptic weights causes neural activity to become unstable to the point that insignificant stimulatory perturbations can trigger chaotic, synchronous network-wide firing known as bursts. This renders the neural network incapable of computing. Since homeostatic plasticity normalizes the synaptic strengths of all neurons in a network, the overall neural network activity stabilizes.
Cortical map
A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students' brains were imaged during the period when they were studying for their exams. In a matter of months, the students' gray matter increased significantly in the posterior and lateral parietal cortex.
Brain healing
Brain injury will commonly be accompanied by acute swelling, which impairs function in brain tissue that remains alive. Resolution of swelling is an important factor for the individual's function to improve. The greatest factor in functional recovery after brain injury comes from the brain's ability to learn, called neuroplasticity. After injury, neuroplasticity allows intact areas of the brain to adapt and attempt to compensate for damaged parts of the brain. Although axons and the peripheral nervous system in the developing brain can regenerate, they cannot in the adult brain. This is partly because of factors produced by cells in the brain that inhibit this regeneration. Dendrites, however, will develop from intact axons, as part of the neuroplasticity process. After severe brain injury, improvement in function related to neuroplasticity is unlikely to occur without help from health professionals skilled in rehabilitation. Recent studies have found collagen is extensively distributed throughout the brain and may be essential in protecting the brain against degeneration such as that in Alzheimers
Synaptic plasticity
The modification of synaptic strength is referred to as functional plasticity. Changes in synaptic strength involve distinct mechanisms of particular types of glial cells, the most researched type being astrocytes.
Hemispherectomy
Along with neuroplasticity, people who undergo hemispherectomies remarkably recover due to resilience. Resilience is the ability, in this case, of the brain being able to recover from a tough situation and take back its shape. Neuroplasticity resilience explains why the hemisphere that is still intact is able to recover many of the functions that were once the removed hemisphere's job. Resilience here is an action in patients with hemispherectomies in which they recover and navigate back to health.
Activity-dependent plasticity
Neurons are the basic functional unit of the brain and process and transmit information through signals. Many different types of neurons can be identified based on their function, such as sensory neurons or motor neurons. Each responds to specific stimuli and sends respective and appropriate chemical signals to other neurons. The basic structure of a neuron is shown here on the right and consists of a nucleus that contains genetic information; the cell body, or the soma, which is equipped with dendritic branches that mostly receive the incoming inputs from other neurons; a long, thin axon that bears axon terminals which carry the output information to other neurons. The dendrites and axons are interfaced through a small connection called a synapse. This component of the neuron contains a variety of chemical messengers and proteins that allow for the transmission of information. It is the variety of proteins and affect of the signal that fundamentally lead to the plasticity feature.
Neuroplasticity
Transcriptional profiling of the frontal cortex of persons ranging from 26 to 106 years of age defined a set of genes with reduced expression after age 40, and especially after age 70. Genes that play central roles in synaptic plasticity were the most significantly affected by age, generally showing reduced expression over time. There was also a marked increase in cortical DNA damage, likely oxidative DNA damage, in gene promoters with aging.
Malleability of intelligence
In the study of malleable intelligence, behavioral factors are often the most intriguing because these are factors humans can seek to control. There are numerous behavioral factors that affect intellectual development and neural plasticity. The key is plasticity, which is caused by experience-driven electrical activation of neurons. This experience-driven activation causes axons to sprout new branches and develop new presynaptic terminals. These new branches often lead to greater mental processing in different areas.
List of medical mnemonics
Neoplastic
Heterosynaptic plasticity
One well studied example of heterosynaptic plasticity is modulatory input-dependent plasticity. Modulatory neurons perform neuromodulation, which is the release of neuromodulators. Neuromodulators differ from classical neurotransmitters. Typically, neuromodulators do not directly generate electrical responses in target neurons. Rather, the release of neuromodulators often alters the efficacy of neurotransmission in nearby chemical synapses. Furthermore, the impact of neuromodulators is often quite long lasting in comparison to classical neurotransmitters.
2,5-Dimethoxy-4-iodoamphetamine
DOI has also been shown to induce rapid growth and reorganization of dendritic spines and synaptic connections with other neurons, processes known to underlie neuroplasticity.
Don Vaughn
Don gave a TEDx talk at UCLA on neuroplasticity, entitled "neurohacking: rewriring your brain".
Memory consolidation
Zif268 is an Immediate Early Gene (IEG) thought to be involved in neuroplasticity by an up-regulation of the transcription factor during REM sleep after pre-exposure to an enriched environment. Results from studies testing the effects of zif268 on mice brains postmortem, suggest that a waking experience prior to sleep can have an enduring effect in the brain, due to an increase of neuroplasticity.
Cellular neuroscience
Synaptic plasticity is the process whereby strengths of synaptic connections are altered. For example, long-term changes in synaptic connection may result in more postsynaptic receptors being embedded in the postsynaptic membrane, resulting in the strengthening of the synapse. Synaptic plasticity is also found to be the neural mechanism that underlies learning and memory. The basic properties, activity and regulation of membrane currents, synaptic transmission and synaptic plasticity, neurotransmission, neuroregensis, synaptogenesis and ion channels of cells are a few other fields studied by cellular neuroscientists. Tissue, cellular and subcellular anatomy are studied to provide insight into mental retardation at the Mental Retardation Research Center MRRC Cellular Neuroscience Core. Journals such as "Frontiers in Cellular Neuroscience" and "Molecular and Cellular Neuroscience" are published regarding cellular neuroscientific topics.
Neuroplasticity
Michael Merzenich is a neuroscientist who has been one of the pioneers of neuroplasticity for over three decades. He has made some of "the most ambitious claims for the field – that brain exercises may be as useful as drugs to treat diseases as severe as schizophrenia – that plasticity exists from cradle to the grave, and that radical improvements in cognitive functioning – how we learn, think, perceive, and remember are possible even in the elderly." Merzenich's work was affected by a crucial discovery made by David Hubel and Torsten Wiesel in their work with kittens. The experiment involved sewing one eye shut and recording the cortical brain maps. Hubel and Wiesel saw that the portion of the kitten's brain associated with the shut eye was not idle, as expected. Instead, it processed visual information from the open eye. It was "…as though the brain didn't want to waste any 'cortical real estate' and had found a way to rewire itself."
Electrophysiological techniques for clinical diagnosis
Spasticity is a velocity dependent resistance to stretch due to increases in gamma motor neuron activity The most commonly affected muscles are those that oppose gravity, the elbow and wrist flexors, knee extensors and ankle plantarflexors. Spasticity is a side effect of multiple central nervous system disorders including Cerebral Palsy, Stroke, Multiple Sclerosis and spinal cord injuries and results in limited joint range of motion of the affected limb.
Einstellung effect
Neurologically, the idea of synaptic plasticity, which is an important neurochemical explanation of memory, can help to understand the Einstellung effect. Specifically, Hebbian theory (which in many regards is the neuroscience equivalent of original associationist theories) is one explanation of synaptic plasticity (Hebb, 1949). It states that when two associated neurons frequently fire together – while infrequently firing apart from one another – the strength of their association tends to become stronger (making future stimulation of one neuron even more likely to stimulate the other). Since the frontal lobe is most often attributed with the roles of planning and problem solving, if there is a neurological pathway which is fundamental to the understanding of Einstellung effect, the majority of it most likely falls within the frontal lobe. Essentially, a Hebbian explanation of Einstellung could be as follows: stimuli are presented in such a way that the subject recognizes him or herself as being in a situation which he or she has been in before. That is, the subject sees, hears, smells, etc., an environment which is akin to an environment which he or she has been in before. The subject then must process the stimuli which are presented in such a way that he or she exhibits a behavior which is appropriate for the situation (be it run, throw, eat, etc.). Because neural growth is, at least in part, due to the associations between two events/ideas, it follows that the more a given stimulus is followed by a specific response, the more likely that in the future that stimulus will invoke the same response. Regarding the Luchins’ experiment, the stimulus presented was a water-jar problem (or to be more technical, the stimulus was a piece of paper which had words and numbers on it which, when interpreted correctly, portray a water-jar problem) and the invoked response was B − A − 2C. While it is a bit of a stretch to assume that there is a direct connection between a "water-jar problem" and "B" − "A" − 2"C" within the brain, it is not unreasonable to assume that the specific neural connections which are active during a water-jar problem-state and those that are active when one thinks “take the second term, subtract the first term, then subtract two of the third term” tend to increase in the amount of overlap as more and more instances where B − A − 2C works are presented.
Personality changes
Negative life events, long-term difficulties, and deteriorated life quality, all predict small but persistent increases in neuroticism, while positive life events, and improved life quality, predict small but persistent decreases in neuroticism. There appears to be no point during the lifespan that neuroticism is immutable, which is known as the plasticity principle.
List of medical mnemonics
Neoplastic
Homeostatic plasticity
Homeostatic plasticity also maintains neuronal excitability in a real-time manner through the coordinated plasticity of threshold and refractory period at voltage-gated sodium channels.
The term homeostatic plasticity derives from two opposing concepts: 'homeostatic' (a product of the Greek words for 'same' and 'state' or 'condition') and plasticity (or 'change'), thus homeostatic plasticity means "staying the same through change".
Activity-dependent plasticity
The future studies and questions for activity-dependent plasticity are nearly endless because the implications of the findings will enable many treatments. Despite many gains within the field, there are a wide variety of disorders that further understanding of activity-dependent mechanisms of plasticity would help treat and perhaps cure. These include autism, different severities of intellectual disability, schizophrenia, Parkinson's disease, stress, and stroke. In addition to a better understanding of the various disorders, neurologists should and will look at the plasticity incurred by the immune system, as it will provide great insight into diseases and also give the basis of new immune-centered therapeutics. A better perspective of the cellular mechanisms that regulate neuronal morphology is the next step to discovering new treatments for learning and memory pathological conditions.
Adult development
New neurons are constantly formed from stem cells in parts of the adult brain throughout adulthood, a process called adult neurogenesis. The hippocampus is the area of the brain that is most active in neurogenesis. Research shows that thousands of new neurons are produced in the hippocampus every day. The brain constantly changes and rewires itself throughout adulthood, a process known as neuroplasticity. Evidence suggests that the brain changes in response to diet, exercise, social environment, stress and toxin intake. These same external factors also influence genetic expression throughout adult life - a phenomenon known as genetic plasticity.
Nonsynaptic plasticity
Intrinsic plasticity is distinct from synaptic plasticity, which involves changes at the synapse between two neurons rather than changes in the electrical properties within a single neuron. There are some closely related phenomena that can affect a neuron's excitability – such as neuromodulation, structural plasticity, short-term plasticity due to channel kinetics, and neural development – but are generally excluded from the term intrinsic plasticity. There is no consensus on the quantity that intrinsic plasticity regulates, e.g. the firing rate of a neuron or its internal calcium concentration. Functionally, intrinsic plasticity might allow neurons to learn the intensity of stimuli and represent those intensity statistics in their excitabilities.
Neural Plasticity (journal)
Neural Plasticity is a peer-reviewed scientific journal covering all aspects of neuroplasticity, especially when concerning its functional involvement in the regulation of behavior and in psychopathology. The journal was established in 1989 as the "Journal of Neural Transplantation" and renamed in 1991 to "Journal of Neural Transplantation and Plasticity", before obtaining its current name in 1998. It is published by Hindawi Publishing Corporation.
Metaplasticity
Metaplasticity is a term originally coined by W.C. Abraham and M.F. Bear to refer to the plasticity of synaptic plasticity. Until that time synaptic plasticity had referred to the plastic nature of "individual" synapses. However this new form referred to the plasticity of the plasticity itself, thus the term "meta"-plasticity. The idea is that the synapse's previous history of activity determines its current plasticity. This may play a role in some of the underlying mechanisms thought to be important in memory and learning such as long-term potentiation (LTP), long-term depression (LTD) and so forth. These mechanisms depend on current synaptic "state", as set by ongoing extrinsic influences such as the level of synaptic inhibition, the activity of modulatory afferents such as catecholamines, and the pool of hormones affecting the synapses under study. Recently, it has become clear that the prior history of synaptic activity is an additional variable that influences the synaptic state, and thereby the degree, of LTP or LTD produced by a given experimental protocol. In a sense, then, synaptic plasticity is governed by an activity-dependent plasticity of the synaptic state; such plasticity of synaptic plasticity has been termed metaplasticity. There is little known about metaplasticity, and there is much research currently underway on the subject, despite its difficulty of study, because of its theoretical importance in brain and cognitive science. Most research of this type is done via cultured hippocampus cells or hippocampal slices.
Neuroplasticity
Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.
Halton Hills Christian School
The Arrowsmith_Program is based on the theory of neuroplasticity. It is now a recognized fact that the brain is pliable and elastic, not fixed as we used to believe. Therefore, it is now possible to physically change the brain in response to stimuli and develop new neural pathways. The exercises created by Barbara Arrowsmith Young over the past 25 years now make it possible for the brains of children with certain learning dysfunctions to be strengthened to the point of average or above-average functionality.
Cortical remapping
Neuroplasticity after a stroke is enabled by new structural and functional circuits that are formed through cortical remapping.
A stroke occurs when there is not enough blood flow to the brain, causing debilitating neurological damage. The tissue that surrounds the infarct (stroke damaged area) has reduced blood flow and is called the penumbra. Though the dendrites in the penumbra have been damaged due to the stroke, they can recover during the restoration of blood flow (reperfusion) if done within hours to a few days of the stroke due to time sensitivity. Due to reperfusion in the peri-infarct cortex (found next to the infarct), the neurons can help with active structural and functional remodelling after stroke.
Neuroplasticity
One recent study of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer. Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in the estrus cycle, females recovered even better. This difference may be attributed to different levels of progesterone, with higher levels of progesterone leading to the faster recovery from brain injury in mice. However, clinical trials showed progesterone offers no significant benefit for traumatic brain injury human patients.
List of medical mnemonics
Neoplastic
Elizabeth Bates
Through her research, Bates demonstrated that neural plasticity allows children with damage to the right hemisphere or the left hemisphere to learn and apply language within a normal range of use. However, when children are matched in age, sex and socioeconomic status, their use is lower than that of children who did not suffer brain damage. The same study presented evidence that brain damage has permanent consequences on language use when incurred as an adult. In a comparative study on the Origins of Language Disorders, Bates found that the period between 0 to 5 years of age was important to the argument of neural plasticity as this suggests that reorganization in response to an injury occurs during this period. However, there are limits to brain plasticity. Despite the area that is damaged, whether it be right-frontal or left-frontal, it increases the risk for expressive language delay within 19 months to 30 months. This suggests that the left-frontal area isn't a unique region that encourages normal language development.
Activity-dependent plasticity
Another pioneer within the field of activity-dependent plasticity is Michael Merzenich, currently a professor in neuroscience at the University of California, San Francisco. One of his contributions includes mapping out and documenting the reorganization of cortical regions after alterations due to plasticity. While assessing the recorded changes in the primary somatosensory cortex of adult monkeys, he looked at several features of the data including how altered schedules of activity from the skin remap to cortical modeling and other factors that affect the representational remodeling of the brain. His findings within these studies have since been applied to youth development and children with language-based learning impairments. Through many studies involving adaptive training exercises on computer, he has successfully designed methods to improve their temporal processing skills. These adaptive measures include word-processing games and comprehension tests that involve multiple regions of the brain in order to answer. The results later translated into his development of the Fast ForWord program in 1996, which aims to enhance cognitive skills of children between kindergarten and twelfth grade by focusing on developing "phonological awareness". It has proven very successful at helping children with a variety of cognitive complications. In addition, it has led to in depth studies of specific complications such as autism and intellectual disability and the causes of them. Alongside a team of scientists, Merzenich helped to provide evidence that autism probes monochannel perception where a stronger stimulus-driven representation dominates behavior and weaker stimuli are practically ignored in comparison.
Karel Svoboda (scientist)
Karel Svoboda (1965 - ) is a neuroscientist on the faculty at the Howard Hughes Medical Institute's Janelia Research Campus. His research focuses on the question of how the neural circuits of the brain produce behavior. He has also performed notable work on neuroplasticity, particularly changes in the brain due to experience and learning.
Viscoplasticity
Viscoplasticity is a theory in continuum mechanics that describes the rate-dependent inelastic behavior of solids. Rate-dependence in this context means that the deformation of the material depends on the rate at which loads are applied. The inelastic behavior that is the subject of viscoplasticity is plastic deformation which means that the material undergoes unrecoverable deformations when a load level is reached. Rate-dependent plasticity is important for transient plasticity calculations. The main difference between rate-independent plastic and viscoplastic material models is that the latter exhibit not only permanent deformations after the application of loads but continue to undergo a creep flow as a function of time under the influence of the applied load.
Connectome
At the beginning of the connectome project, it was thought that the connections between neurons were unchangeable once established and that only individual synapses could be altered. However, recent evidence suggests that connectivity is also subject to change, termed neuroplasticity. There are two ways that the brain can rewire: formation and removal of synapses in an established connection or formation or removal of entire connections between neurons. Both mechanisms of rewiring are useful for learning completely novel tasks that may require entirely new connections between regions of the brain. However, the ability of the brain to gain or lose entire connections poses an issue for mapping a universal species connectome.
Neuroplasticity
This implied neuroplasticity during the critical period. However, Merzenich argued that neuroplasticity could occur beyond the critical period. His first encounter with adult plasticity came when he was engaged in a postdoctoral study with Clinton Woosley. The experiment was based on observation of what occurred in the brain when one peripheral nerve was cut and subsequently regenerated. The two scientists micromapped the hand maps of monkey brains before and after cutting a peripheral nerve and sewing the ends together. Afterwards, the hand map in the brain that they expected to be jumbled was nearly normal. This was a substantial breakthrough. Merzenich asserted that, "If the brain map could normalize its structure in response to abnormal input, the prevailing view that we are born with a hardwired system had to be wrong. The brain had to be plastic." Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."
Nonsynaptic plasticity
Nonsynaptic activity in the cell is usually expressed as changes in neuronal excitability. This occurs through modulation of membrane components, such as resting and voltage-gated channels and ion pumps. Nonsynaptic processes are thought to be involved in memory storage. One possible mechanism of this action involves marking a neuron that has been recently active with changes in excitability. This would help to link temporally separated stimuli. Another potential mechanism comes from a computational model that indicates that nonsynaptic plasticity may prime circuits for modification in learning because excitability changes may regulate the threshold for synaptic plasticity.
Paul Bach-y-Rita
Bach-y-Rita's most notable work was in the field of neuroplasticity. He is seen as the first to propose the concept of sensory substitution to treat patients with disabilities, often those caused by neurological problems. One of the first applications of sensory substitution he created was a chair which allowed blind people to 'see'.
The trials he conducted in 1969
are now regarded to be the first form of experimental evidence for neuroplasticity and the feasibility of sensory substitution. Later in his career, Bach-y-Rita created a device which enabled patients with damaged vestibular nuclei to regain their ability to remain balanced, by using an electrical stimulator placed on the tongue which reacted to a motion sensor affixed to the patient. This application enabled patients to remain balanced without the equipment after several weeks use.
Developmental plasticity
During development, the central nervous system acquires information via endogenous or exogenous factors as well as learning experiences. In acquiring and storing such information, the plastic nature of the central nervous system allows for the adaptation of existing neural connections in order to accommodate new information and experiences, resulting in developmental plasticity. This form of plasticity that occurs during development is the result of three predominant mechanisms: synaptic and homeostatic plasticity, and learning.
Neuroplasticity
Studies in people recovering from stroke also provided support for neuroplasticity, as regions of the brain remained healthy could sometimes take over, at least in part, functions that had been destroyed; Shepherd Ivory Franz did work in this area.
Nonsynaptic plasticity
The storage capacity of synaptic-based memory storage systems is very large, making it an attractive mechanism to study. There are approximately 10 synapses per neuron and 10 neurons in the human brain. Nonsynaptic plasticity is often overlooked simply because its storage capacity is not as high. Regulating the density of ion channels in the axon and soma of a neuron would change the throughput and affect all of the synapses. Therefore, its storage capacity would be significantly less than that of synaptic plasticity.
Neuroplasticity
Other significant evidence was produced in the 1960s and after, notably from scientists including Paul Bach-y-Rita, Michael Merzenich along with Jon Kaas, as well as several others.
Neuralgia
By understanding the neuroplastic changes following nerve damage, researchers may be able to gain a better understanding of the mechanism of hyperexcitability in the nervous system that is believed to cause neuropathic pain.
Nonsynaptic plasticity
One mechanism for preserving the dynamic range of a neuron is synaptic scaling, the homeostatic form of plasticity that restores neuronal activity to its normal 'baseline' levels by changing the postsynaptic response of all the synapses of a neuron as a function of activity. This means that the same scaling is done to each synapse, to either strengthen or weaken all of a neuron’s connections. Scaling can be multiplicative (multiplying or dividing the strength of each synapse by a constant number) or additive (adding or subtracting the same value from the synaptic weight). Homeostatic mechanisms go beyond the synapse. Modulation of the intrinsic excitability of a neuron is a way to maintain stability despite changing numbers and strengths of synapses. Cultured cortical pyramidal neurons maintain stability through the regulation of ionic conductances. The regulation of ionic conductances is achieved through the controlled release of brain-derived neurotrophic factor (BDNF). BDNF has also been found to influence synaptic scaling, suggesting that this neurotrophic factor may be responsible for the coordination of synaptic and nonsynaptic mechanisms in homeostatic plasticity.
Alzheimer's disease research
Neuronal plasticity is a key player in cognitive function that cannot be ignored in study of AD progression. Microarray studies found that NEFM, NEFL, and SV2B are highly downregulated in samples obtained from severe AD patients. NEFL is a neurofilament gene that has been shown to be related to hypotrophy of axons in motorneurons when mutated. However, both neurofilaments (NEFL and NEFM) have been documented to be involved in neurological disease, Charcot-Marie-Tooth, instead of AD, which demonstrate possible unknown connections of AD to other neurological diseases. SV2B is another gene that is downregulated in AD and has been shown to be related to neurodegeneration, particularly synaptic calcium-regulated exocytosis. The downregulation of genes responsible for neural synapse and neuroplasticity is related to another family of protein that has been found to be related to AD pathogenesis, EGR (early growth response). This EGR is regulated by upregulated FOXO1 (Forkhead Box O1) through PI3K/Akt pathway, which is listed as one of the pathway for future in anti-AD medication. These findings using computational methods allow for the connection of different studies and facilitate the understanding of disease complexity as well as directing to new possible biomarkers of AD.
Synaptic scaling
In neuroscience, synaptic scaling (or homeostatic scaling) is a form of homeostatic plasticity, in which the brain responds to chronically elevated activity in a neural circuit with negative feedback, allowing individual neurons to reduce their overall action potential firing rate. Where Hebbian plasticity mechanisms modify neural synaptic connections selectively, synaptic scaling normalizes all neural synaptic connections by decreasing the strength of each synapse by the same factor (multiplicative change), so that the relative synaptic weighting of each synapse is preserved.Synaptic scaling is a post-synaptic homeostatic plasticity mechanism that takes place with changes in the quantity of AMPA receptors at a post-synaptic terminal (the tip of the dendrite belonging to the post-synaptic neuron that meets with the tip of an axon belonging to the pre-synaptic neuron) of a neuron. This closed-loop process gives a neuron the ability to have global negative feedback control of synaptic strength of all its synaptic connections by altering the probability of glutamate (the most common excitatory neurotransmitter) making contact with post-synaptic AMPA receptors. Therefore, a neuron's ability to modulate the quantity of post-synaptic AMPA receptors gives it the ability to achieve a set action potential firing rate.
Pixel artist
Neuroplasticity is a key element of observing many pixel images. While two individuals will observe the same photons reflecting off a photorealistic image and hitting their retinas, someone whose mind has been primed with the theory of pointillism may "see" a very different image as the image is interpreted in the visual cortex.
Nonsynaptic plasticity
Synaptic plasticity is the ability of a synapse between two neurons to change in strength over time. Synaptic plasticity is caused by changes in use of the synaptic pathway, namely, the frequency of synaptic potentials and the receptors used to relay chemical signals. Synaptic plasticity plays a large role in learning and memory in the brain. Synaptic plasticity can occur through intrinsic mechanisms, in which changes in synapse strength occur because of its own activity, or through extrinsic mechanisms, in which the changes in synapse strength occur via other neural pathways. Short-term inhibitory synaptic plasticity often occurs because of limited neurotransmitter supply at the synapse, and long-term inhibition can occur through decreased receptor expression in the postsynaptic cell. Short-term complementary synaptic plasticity often occurs because of residual or increased ion flow in either the presynaptic or postsynaptic terminal, while long-term synaptic plasticity can occur through the increased production of AMPA and NMDA glutamate receptors, among others, in the postsynaptic cell.
Neuregulin 1
Neuregulin 1 is thought to play a role in synaptic plasticity. It has been shown that a loss of Neuregulin 1 within cortical projection neurons results in increased inhibitory connections and reduced synaptic plasticity. Similarly, overexpression of Neuregulin 1 results in disrupted excitatory-inhibitory connections, reduced synaptic plasticity, and abnormal dendritic spine growth. Mutations in human L1 cell adhesion molecules are reported to cause a number of neuronal disorders. In addition, recent research in Drosophila model has also shown Nrg's involvement in regulating dendritic pruning in ddaC neurons in a Rab5/ESCRT-mediated endocytic pathway. Thus, careful regulation of the amount of Neuregulin 1 must be maintained in order to preserve an intricate balance between excitatory and inhibitory connections within the central nervous system (CNS). Any disruption in this inhibitory system may contribute to impaired synaptic plasticity, a symptom endemic in schizophrenic patients.
Constraint-induced movement therapy
As a result of the patient engaging in repetitive exercises with the affected limb, the brain grows new neural pathways. This change in the brain is referred to as cortical reorganization or neuroplasticity. One study by Deluca et al. showed that using transcranial magnetic stimulation (TMS) that the excitable cortex of the affected cortex in adults patients with HCP doubled in size after 12 days of therapy. Recently, the possible benefits of cortical reorganization has led to studies of CIMT on children because neuroplasticity is even greater among children than adults. Particular interest is growing in CIMT for children who have cerebral palsy where one arm is more affected than the other.
Sensory stimulation therapy
Brain plasticity refers to the ability of the brain to restructure itself, form new connections, or adjust the strength of existing connections. The current paradigm allow for conceptualization of brain that is capable of change. Various researchers are using this concept to develop new therapies for conditions that were previously viewed as permanent; for example Paul Bach-y-Rita has worked on devices to give sight to blind individuals, and alleviate a feeling of falling in a patient that has lost function of the vestibular apparatus.
Metaplasticity
The brain is "plastic", meaning it can be molded and formed. This plasticity is what allows you to learn throughout your lifetime; your synapses change based on your experience. New synapses can be made, old ones destroyed, or existing ones can be strengthened or weakened. The original theory of plasticity is called "Hebbian plasticity", named after Donald Hebb in 1949. A quick but effective summary of Hebbian theory is that "cells that fire together, wire together", together being the key word here which will be explained shortly. Hebb described an early concept of the theory, not the actual mechanics themselves. Hebbian plasticity involves two mechanisms: LTP and LTD, discovered by Bliss and Lomo in 1973. LTP, or long-term potentiation, is the increase of synapse sensitivity due to a prolonged period of activity in both the presynaptic and postsynaptic neuron. This prolonged period of activity is normally concentrated electric impulses, usually around 100 Hz. It is called "coincidence" detection in that it only strengthens the synapse if there was sufficient activity in both the presynaptic and postsynaptic cells. If the postsynaptic cell does not become sufficiently depolarized then there is no coincidence detection and LTP/LTD do not occur. LTD, or long-term depression, works the same way however it focuses on a lack of depolarization coincidence. LTD can be induced by electrical impulses at around 5 Hz. These changes are synapse specific. A neuron can have many different synapses all controlled via the same mechanisms defined here.
Synaptic plasticity
In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.
Neuroplasticity
In 1945, Justo Gonzalo concluded from his research of brain dynamics, that, contrary to the activity of the projection areas, the "central" cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a "maneuvering mass", rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties. He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment, and specially, several first-hand brain injuries cases in which he observed dynamic and adaptive properties in their disorders, in particular in the inverted perception disorder [e.g., see pp 260–62 Vol. I (1945), p 696 Vol. II (1950)]. He stated that a sensory signal in a projection area would be only an inverted and constricted outline that would be magnified due to the increase in recruited cerebral mass, and re-inverted due to some effect of brain plasticity, in more central areas, following a spiral growth.
Postherpetic neuralgia
A key factor in the neural plasticity underlying neuropathic pain is altered gene expression in sensory dorsal root ganglia neurons. Injury to sensory nerves induces neurochemical, physiological, and anatomical modifications to afferent and central neurons, such as afferent terminal sprouting and inhibitory interneuron loss. Following nerve damage, NaCl channel accumulation causes hyperexcitability, and downregulation of the TTX-resistant Nav1.8 (sensory neuron specific, SNS1) channel and upregulation of TTX-sensitive Nav1.3 (brain type III) and TRPV1 channels. These changes contribute to increased NMDA glutamate receptor-dependent excitability of spinal dorsal horn neurons and are restricted to the ipsilateral (injured) side. A combination of these factors could contribute to the neuropathic pain state of postherpetic neuralgia.
Neuroplasticity
Neuroplasticity, also known as brain plasticity, neuroelasticity, or neural plasticity, is the ability of the brain to change throughout an individual's life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time. Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are "plastic") even through adulthood. However, the developing brain exhibits a higher degree of plasticity than the adult brain.
Global aphasia
When evaluating the prognosis of a patient, the main contributing participant factors that influence the extent of neuroplasticity, or the brain's ability to change are: age, lesion location, pre-existing cognitive status, motivation, age, overall health, and interaction amongst these. After brain damage, initial signs of global aphasia may appear within the first two days due to brain swelling (cerebral edema). With some time and natural recovery, impairment presentation may progress into expressive aphasia (most commonly) or receptive aphasia. Due to the size and location of the lesion associated with global aphasia, the prognosis for language abilities is poor. Research has shown that the prognosis of long-term language abilities is determined by the initial severity level of aphasia within the first four weeks after a stroke. As a result, there is a poor prognosis for persons who retain a diagnosis of aphasia after one month due to limited initial language abilities. Nonetheless, in the first year post-stroke, patients with global aphasia showed improvement in their Western Aphasia Battery (WAB) scores from baseline. When compared to individuals with Broca’s, Wernicke’s, anomic, and conduction types of aphasia, those with Broca’s aphasia showed the best rate and extent of improvement followed by global aphasia. The rate of improvement in language function was highest in the first four weeks after stroke.
Biological basis of personality
Synaptic plasticity refers to the ability of neurons to strengthen or weaken the connections between them. According to Hebbian theory, these connections are strengthened and maintained through repeated stimulation between neurons. Specifically, there is an emphasis on long-term potentiation (LTP), which is the prolonged strengthening of synaptic connections that facilitate learning from experience.
Synaptic plasticity
where formula_2 is the synaptic weight of the formula_3th input axon, formula_4 is a time constant dependent on the insertion and removal rates of neurotransmitter receptors, which is dependent on formula_5, the concentration of calcium. formula_6 is also a function of the concentration of calcium that depends linearly on the number of receptors on the membrane of the neuron at some fixed point. Both formula_7 and formula_4 are found experimentally and agree on results from both hypotheses. The model makes important simplifications that make it unsuited for actual experimental predictions, but provides a significant basis for the hypothesis of a calcium-based synaptic plasticity dependence.
Activity-dependent plasticity
It is known that during postnatal life a critical step to nervous system development is synapse elimination. The changes in synaptic connections and strength are results from LTP and LTD and are strongly regulated by the release of brain-derived neurotrophic factor (BDNF), an activity-dependent synapse-development protein. In addition to BDNF, Nogo-66 receptors, and more specifically NgR1, are also involved in the development and regulation of neuronal structure. Damage to this receptor leads to pointless LTP and attenuation of LTD. Both situations imply that NgR1 is a regulator of synaptic plasticity. From experiments, it has been found that stimulation inducing LTD leads to a reduction in synaptic strength and loss of connections but, when coupled simultaneously with low-frequency stimulation, helps the restructuring of synaptic contacts. The implications of this finding include helping people with receptor damage and providing insight into the mechanism behind LTP.
Kinesiology
Neuroplasticity is also a key scientific principle used in kinesiology to describe how movement and changes in the brain are related. The human brain adapts and acquires new motor skills based on this principle, which includes both adaptive and maladaptive brain changes.
Cross modal plasticity
Cross modal plasticity is the adaptive reorganization of neurons to integrate the function of two or more sensory systems. Cross modal plasticity is a type of neuroplasticity and often occurs after sensory deprivation due to disease or brain damage. The reorganization of the neural network is greatest following long-term sensory deprivation, such as congenital blindness or pre-lingual deafness. In these instances, cross modal plasticity can strengthen other sensory systems to compensate for the lack of vision or hearing. This strengthening is due to new connections that are formed to brain cortices that no longer receive sensory input.
Activity-dependent plasticity
The idea of neural plasticity was first proposed during 1890 by William James in Principles of Psychology. During the first half of the 1900s, the word 'plasticity' was directly and indirectly rejected throughout science. Many scientists found it hard to receive funding because nearly everyone unanimously supported the fact that the brain was fully developed at adulthood and specific regions were unable to change functions after the critical period. It was believed that each region of the brain had a set and specific function. Despite this, several pioneers pushed the idea of plasticity through means of various experiments and research. There are others that helped to the current progress of activity-dependent plasticity but the following contributed very effective results and ideas early on.
NOMFET
NOMFET is a nanoparticle organic memory field-effect transistor. The transistor is designed to mimic the feature of the human synapse known as plasticity, or the variation of the speed and strength of the signal going from neuron to neuron. The device uses gold nano-particles of about 5—20 nm set with pentacene to emulate the change in voltages and speed within the signal. This device uses charge trapping/detrapping in an array of gold nanoparticules (NPs) at the SiO2/pentacene interface to design a SYNAPSTOR (synapse transistor) mimicking the dynamic plasticity of a biological synapse. This device (memristor-like) mimics short-term plasticity (STP) and temporal correlation plasticity (STDP, spike-timing dependent plasticity), two "functions" at the basis of learning processes. A compact model was developed, and these organic synapstors were used to demonstrate an associative memory, which can be trained to present a pavlovian response. A recent report showed that these organic synapse-transistors (synapstor) are working at 1 volt and with a plasticity typical response time in the range 100-200 ms. The device also works in contact with an electrolyte (EGOS : electrolyte gated organic synapstor) and can be interfaced with biologic neurons.
Neuroplasticity
In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body. The authors stated that: "In fact, this finding extends our understanding of the brain's plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms—the brain truly does change itself."
Neuroplasticity
Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization. For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth. Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus. However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.
Nonsynaptic plasticity
Savings is the ability to relearn forgotten information much faster than it was learned originally. Nonsynaptic plasticity is a possible mechanism for this savings effect. During training procedures many neurons experience an increase in intrinsic excitability. This increase in excitability persists even after the memory fades.
Wendy Suzuki
Suzuki joined the faculty at New York University's Center for Neural Science in 1998. Her research interests center on neuroplasticity and how the brain is able to change and adapt over the course of a person's life. Her early career research focused on the areas of the brain that play an important role in our ability to form and retain memories. More recently, she's expanded this work to study the role of aerobic exercise on potentially enhancing cognitive abilities.
Adult neurogenesis
Some studies have hypothesized that learning and memory are linked to depression, and that neurogenesis may promote neuroplasticity. One study proposes that mood may be regulated, at a base level, by plasticity, and thus "not chemistry". Accordingly, the effects of antidepressant treatment would only be secondary to change in plasticity. However another study has demonstrated an interaction between antidepressants and plasticity; the antidepressant fluoxetine has been shown to restore plasticity in the adult rat brain. The results of this study imply that instead of being secondary to changes in plasticity, antidepressant therapy could promote it.
Neuroplasticity
Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also part of the somatosensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. The work of Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations causing a substantial impact on the cortical plasticity in that system.
Neurofeedback
In 2010, a study provided some evidence of neuroplastic changes occurring after brainwave training. Half an hour of voluntary control of brain rhythms led in this study to a lasting shift in cortical excitability and intracortical function. The authors observed that the cortical response to transcranial magnetic stimulation (TMS) was significantly enhanced after neurofeedback, persisted for at least 20 minutes, and was correlated with an EEG time-course indicative of activity-dependent plasticity.
Memory improvement
Experience-dependent neuroplasticity suggests that the brain changes in response to what it experiences. London taxicab drivers provide a great example of this dynamic. They undergo extensive training for 2–4 years, learning and memorizing street names, layout of streets within the city and the quickest cross-city routes. After studying London taxicab drivers over a period of time, it was found that the grey matter volume increased over time in the posterior hippocampus, an area in the brain involved heavily in memory. The longer taxi drivers navigated the streets of London, the greater the posterior hippocampal gray matter volume. This suggests a correlation between a healthy person's mental training or exercise and their brains capacity to manage greater volume and more complex information. It should be noted, however, that the increase in volume actually led to a "decrease" in the taxi drivers' ability to acquire new visuo-spatial information.
Nonsynaptic plasticity
Nonsynaptic plasticity, can function to alleviate the effects of brain damage. When one of the vestibular nerves is damaged, disparity in the firing rates of neurons in the vestibular nuclei causes unnecessary vestibular reflexes. The symptoms of this damage fade over time. This is likely due to modifications of intrinsic excitability in the neurons of the vestibular nucleus.
Developmental plasticity
The formation of the nervous system is one of the most crucial events in the developing embryo. Specifically, the differentiation of stem cell precursors into specialized neurons gives rise to the formation of synapses and neural circuits, which is key to the principle of plasticity. During this pivotal point in development, consequent developmental processes like the differentiation and specialization of neurons are highly sensitive to exogenous and endogenous factors. For example, in utero exposure to nicotine has been linked to adverse effects such as severe physical and cognitive deficits as a result of impeding the normal activation of acetylcholine receptors. In a recent study, the connection between such nicotine exposure and prenatal development was assessed. It was determined that nicotine exposure in early development can have a lasting and encompassing effect on neuronal structures, underlying the behavioral and cognitive defects observed in exposed humans and animals. Additionally, by disrupting proper synaptic function through nicotine exposure, the overall circuit may become less sensitive and responsive to stimuli, resulting in compensatory developmental plasticity. It is for this reason that exposure to various environmental factors during developmental periods can cause profound effects on subsequent neural functioning.
Memory improvement
Neuroplasticity is the mechanism by which the brain encodes experience, learns new behaviours and relearns lost behaviour if the brain has been damaged.
Perineuronal net
Epilepsy is a chronic neurological disorder characterized by abnormal electrical activity in the brain. This abnormal electrical activity results in increased plastic changes that play a part of the pathogenesis of the disease. Following seizures, there is a decrease in phosphacan and phosphacan-positive PNNs and an increase in cleaved brevican in the temporal lobe and hippocampus. Seizures also increase the amount of full-length neurocan, a CSPG only found in the neonatal brain. This degradation of CSPGs and PNNs could be responsible for the increased plasticity associated with the disorder.