Neuroplasticity, also known asneural plasticity or justplasticity, is the medium ofneural networks in thebrain to change throughgrowth and reorganization. Neuroplasticity refers to the brain's ability to reorganize and rewire its neural connections, enabling it to adapt and function in ways that differ from its prior state. This process can occur in response to learning new skills, experiencing environmental changes, recovering from injuries, or adapting to sensory or cognitive deficits. Such adaptability highlights the dynamic and ever-evolving nature of the brain, even into adulthood.[1] These changes range from individualneuron pathways making new connections, to systematic adjustments likecortical remapping orneural oscillation. Other forms of neuroplasticity include homologous area adaptation, cross modal reassignment, map expansion, and compensatory masquerade.[2] Examples of neuroplasticity includecircuit and network changes that result fromlearning a new ability,information acquisition,[3] environmental influences,[4] pregnancy,[5] caloric intake,[6] practice/training,[7] andpsychological stress.[8]
Neuroplasticity was once thought byneuroscientists to manifest only during childhood,[9][10] but research in the later half of the 20th century showed that many aspects of the brain exhibit plasticity through adulthood.[11] The developing brain exhibits a higher degree of plasticity than the adult brain.[12]Activity-dependent plasticity can have significant implications for healthy development, learning,memory, and recovery frombrain damage.[13][14][15]
The termplasticity was first applied to behavior in 1890 byWilliam James inThe Principles of Psychology where the term was used to describe "a structure weak enough to yield to an influence, but strong enough not to yield all at once".[16][17] The first person to use the termneural plasticity appears to have been the Polish neuroscientistJerzy Konorski.[11][18]
One of the first experiments providing evidence for neuroplasticity was conducted in 1793, by Italian anatomistMichele Vincenzo Malacarne, who described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. Malacarne discovered that the cerebellums of the trained animals were substantially larger than the cerebellum of the untrained animals. However, while these findings were significant, they were eventually forgotten.[19] In 1890, the idea that the brain and its function are not fixed throughout adulthood was proposed byWilliam James inThe Principles of Psychology, though the idea was largely neglected.[17] Up until the 1970s, neuroscientists believed that the brain's structure and function was essentially fixed throughout adulthood.[20]
While the brain was commonly understood as a nonrenewable organ in the early 1900s, the pioneering neuroscientistSantiago Ramón y Cajal used the term neuronal plasticity to describe nonpathological changes in the structure of adult brains. Based on his renownedneuron doctrine, Cajal first described the neuron as the fundamental unit of the nervous system that later served as an essential foundation to develop the concept of neural plasticity.[21] Many neuroscientists used the term plasticity to explain the regenerative capacity of theperipheral nervous system only. Cajal, however, used the term plasticity to reference his findings of degeneration and regeneration in the adult brain (a part of thecentral nervous system). This was controversial, with some likeWalther Spielmeyer andMax Bielschowsky arguing that the CNS cannot produce new cells.[22][23]
The term has since been broadly applied:
Given the central importance of neuroplasticity, an outsider would be forgiven for assuming that it was well defined and that a basic and universal framework served to direct current and future hypotheses and experimentation. Sadly, however, this is not the case. While many neuroscientists use the word neuroplasticity as an umbrella term it means different things to different researchers in different subfields ... In brief, a mutually agreed-upon framework does not appear to exist.[24]
In 1923,Karl Lashley conducted experiments onrhesus monkeys that demonstrated changes in neuronal pathways, which he concluded were evidence of plasticity. Despite this, and other research that suggested plasticity, neuroscientists did not widely accept the idea of neuroplasticity.
Inspired by work fromNicolas Rashevsky,[25] in 1943,McCulloch andPitts proposed theartificial neuron, with a learning rule, whereby new synapses are produced when neurons fire simultaneously.[26] This is then extensively discussed inThe organization of behavior (Hebb, 1949) and is now known asHebbian learning.
In 1945,Justo Gonzalo concluded from his research on brain dynamics, that, contrary to the activity of theprojection 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.[27] He gives as a first example of adaptation, to see upright with reversing glasses in theStratton experiment,[28] 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)].[27] 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.[29]
Marian Diamond of the University of California, Berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964.[30][31]
Other significant evidence was produced in the 1960s and after, notably from scientists includingPaul Bach-y-Rita,Michael Merzenich along withJon Kaas, as well as several others.[20][32] An attempt to describe the mechanisms of neuroplasticity, an early version of thecomputational theory of mind derived from Hebb's work, was put forward by Peter Putnam andRobert W. Fuller in that time.[33][34]
In the 1960s,Paul Bach-y-Rita invented a device that was tested on a small number of people, and involved a person sitting in a chair, embedded in which were nubs that were made to vibrate in ways that translated images received in a camera, allowing a form of vision viasensory substitution.[35][36]
Studies in people recovering fromstroke also provided support for neuroplasticity, as regions of the brain that remained healthy could sometimes take over, at least in part, functions that had been destroyed;Shepherd Ivory Franz did work in this area.[37][38]
Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London's layout in local taxi drivers.[39][40][41] 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.
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."[35] Merzenich's work was affected by a crucial discovery made byDavid Hubel andTorsten 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."[35]
This implied neuroplasticity during thecritical 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."[35] Merzenich received the 2016Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."[42]
There are different ideas and theories on what biological processes allow for neuroplasticity to occur. The core of this phenomenon is based upon synapses and how connections between them change based on neuron functioning. It is widely agreed upon that neuroplasticity takes on many forms, as it is a result of a variety of pathways. These pathways, mainly signaling cascades, allow for gene expression alterations that lead to neuronal changes, and thus neuroplasticity.
There are a number of other factors that are thought to play a role in the biological processes underlying the changing of neural networks in the brain. Some of these factors include synapse regulation viaphosphorylation, the role of inflammation and inflammatory cytokines, proteins such as Bcl-2 proteins and neutrophorins, and energy production viamitochondria.[43]
JT Wall and J Xu have traced the mechanisms underlying neuroplasticity. Re-organization is not corticallyemergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex.[44]
Christopher Shaw and Jill McEachern (eds) in "Toward a theory of Neuroplasticity", state that there is no all-inclusive theory that overarches different frameworks and systems in the study of neuroplasticity. However, researchers often describe neuroplasticity as "the ability to make adaptive changes related to the structure and function of the nervous system."[45] Correspondingly, two types of neuroplasticity are often discussed: structural neuroplasticity and functional neuroplasticity.
Structural plasticity is often understood as the brain's ability to change its neuronal connections. The changes ofgrey matter proportion or the synaptic strength in the brain are considered as examples of structural neuroplasticity. This type of neuroplasticity often studies the effect of various internal or external stimuli on the brain's anatomical reorganization. New neurons are constantly produced and integrated into the central nervous system based on this type of neuroplasticity.[46] Researchers nowadays use multiple cross-sectional imaging methods (i.e.magnetic resonance imaging (MRI),computerized tomography (CT)) to study the structural alterations of the human brains.[47] Structural neuroplasticity is currently investigated more within the field of neuroscience in current academia.[21] Adult neurogenesis "has not been convincingly demonstrated in humans".[46]
Functional plasticity refers to the brain's ability to alter and adapt the functional properties of network of neurons. It can occur in four known ways namely:
Homologous area adaptation is the assumption of a particular cognitive process by a homologous region in the opposite hemisphere.[48] For instance, through homologous area adaptation a cognitive task is shifted from a damaged part of the brain to its homologous area in opposite side of the brain. Homologous area adaptation is a type of functional neuroplasticity that occur usually in children rather than adults.
In map expansion, cortical maps related to particular cognitive tasks expand due to frequent exposure to stimuli. Map expansion has been proven through experiments performed in relation to the study: experiment on effect of frequent stimulus on functional connectivity of the brain was observed in individuals learning spatial routes.[49]
Cross-model reassignment involves reception of novel input signals to a brain region which has been stripped off its default input.
Functional plasticity through compensatory masquerade occurs using different cognitive processes for an already established cognitive task when the initial process cannot be followed due to impairment.
Changes in the brain associated with functional neuroplasticity can occur in response to two different types of events:
In the latter case the functions from one part of the brain transfer to another part of the brain based on the demand to produce recovery of behavioral or physiological processes.[50] Regarding physiological forms of activity-dependent plasticity, those involving synapses are referred to assynaptic plasticity. The strengthening or weakening of synapses that results in an increase or decrease of firing rate of the neurons are calledlong-term potentiation (LTP) andlong-term depression (LTD), respectively, and they are considered as examples of synaptic plasticity that are associated with memory.[51] Thecerebellum is a typical structure with combinations of LTP/LTD and redundancy within the circuitry, allowing plasticity at several sites.[52] More recently it has become clearer that synaptic plasticity can be complemented by another form of activity-dependent plasticity involving the intrinsic excitability of neurons, which is referred to asintrinsic plasticity.[53][54][55] This, as opposed tohomeostatic plasticity does not necessarily maintain the overall activity of a neuron within a network but contributes to encoding memories.[56] Also, many studies have indicated functional neuroplasticity in the level of brain networks, where training alters the strength of functional connections.[57][58] Although a recent study discusses that these observed changes should not directly relate to neuroplasticity, since they may root in the systematic requirement of the brain network for reorganization.[59]
The adult brain is not entirely "hard-wired" with fixedneuronal circuits. There are many instances of cortical and subcortical rewiring of neuronal circuits in response to training as well as in response to injury.
There is ample evidence[60] for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures including the cerebral cortex.[61] The specific details of how this process occurs at the molecular andultrastructural levels are topics of active neuroscience research. The way experience can influence the synaptic organization of the brain is also the basis for a number of theories of brain function including the general theory of mind andneural Darwinism. The concept of neuroplasticity is also central to theories of memory and learning that are associated with experience-driven alteration of synaptic structure and function in studies ofclassical conditioning in invertebrate animal models such asAplysia.
There is evidence thatneurogenesis (birth of brain cells) occurs in the adult, rodent brain—and such changes can persist well into old age.[62] The evidence for neurogenesis is mainly restricted to thehippocampus andolfactory bulb, but research has revealed that other parts of the brain, including the cerebellum, may be involved as well.[63] However, the degree of rewiring induced by the integration of new neurons in the established circuits is not known, and such rewiring may well be functionally redundant.[64]
A surprising consequence of neuroplasticity is that the brain activity associated with a given function can be transferred to a different location; this can result from normal experience and also occurs in the process of recovery from brain injury. Neuroplasticity is the fundamental issue that supports the scientific basis for treatment ofacquired brain injury with goal-directed experiential therapeutic programs in the context ofrehabilitation approaches to the functional consequences of the injury.
Neuroplasticity is gaining popularity as a theory that, at least in part, explains improvements in functional outcomes with physical therapy post-stroke. Rehabilitation techniques that are supported by evidence which suggest cortical reorganization as the mechanism of change includeconstraint-induced movement therapy,functional electrical stimulation, treadmill training with body-weight support, andvirtual reality therapy.Robot assisted therapy is an emerging technique, which is also hypothesized to work by way of neuroplasticity, though there is currently insufficient evidence to determine the exact mechanisms of change when using this method.[65]
One group has developed a treatment that includes increased levels ofprogesterone injections in brain-injured patients. "Administration of progesterone after traumatic brain injury[66] (TBI) and stroke reducesedema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory-motor recovery."[67] In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections.[68] However, a study published in theNew England Journal of Medicine in 2014 detailing the results of a multi-center NIH-funded phase III clinical trial of 882 patients found that treatment of acute traumatic brain injury with the hormone progesterone provides no significant benefit to patients when compared with placebo.[69]
For decades, researchers assumed that humans had to acquirebinocular vision, in particularstereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons withamblyopia,convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements andstereopsis recovery are now active areas of scientific and clinical research.[70][71][72]
In the phenomenon ofphantom limb sensation, a person continues to feel pain or sensation within a part of their body that has beenamputated. This is strangely common, occurring in 60–80% of amputees.[73] Anexplanation for this is based on the concept of neuroplasticity, as thecortical maps of the removed limbs are believed to have become engaged with the area around them in thepostcentral 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.
The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990sV.S. Ramachandran theorized that phantom limbs were the result ofcortical remapping. However, in 1995 Herta Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain.[74] Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.[75] This phenomenon is sometimes referred to as maladaptive plasticity.
In 2009, Lorimer Moseley and Peter Brugger carried out an experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible[clarification needed] 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.[76]
Individuals who have 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 andinflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolongednociception from the periphery then elicits a neuroplastic response at the cortical level to change itssomatotopic organization for the painful site, inducingcentral sensitization.[77] For instance, individuals experiencingcomplex 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.[78] Additionally, chronic pain has been reported to significantly reduce the volume ofgrey matter in the brain globally, and more specifically at theprefrontal cortex and rightthalamus.[79] 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,[80]chronic low back pain[81] andcarpal tunnel syndrome.[82]
A number of studies have linked meditation practice to differences in cortical thickness or density ofgray matter.[83][84][85][86] One of the most well-known studies to demonstrate this was led bySara Lazar, from Harvard University, in 2000.[87]Richard Davidson, a neuroscientist at theUniversity of Wisconsin, has led experiments in collaboration with theDalai Lama on effects of meditation on the brain. His results suggest that meditation may lead to change in the physical structure of brain regions associated withattention,anxiety,depression,fear,anger, and compassion as well as the ability of the body to heal itself.[88][89]
There is substantial evidence that artistic engagement in a therapeutic environment can create changes in neural network connections as well as increase cognitive flexibility.[90][91] In one 2013 study, researchers found evidence that long-term, habitual artistic training (e.g. musical instrument practice, purposeful painting, etc.) can "macroscopically imprint a neural network system of spontaneous activity in which the related brain regions become functionally and topologically modularized in both domain-general and domain-specific manners".[92] In simple terms, brains repeatedly exposed to artistic training over long periods develop adaptations to make such activity both easier and more likely to spontaneously occur.
Some researchers and academics have suggested that artistic engagement has substantially altered the human brain throughout our evolutionary history. D.W Zaidel, adjunct professor of behavioral neuroscience and contributor atVAGA, has written that "evolutionary theory links the symbolic nature of art to critical pivotal brain changes inHomo sapiens supporting increased development of language and hierarchical social grouping".[93]
There is evidence that engaging in music-supported therapy can improve neuroplasticity in patients who are recovering from brain injuries. Music-supported therapy can be used for patients that are undergoing stroke rehabilitation where a one month study of stroke patients participating in music-supported therapy showed a significant improvement in motor control in their affected hand.[94] Another finding was the examination of grey matter volume of adults developingbrain atrophy and cognitive decline where playing a musical instrument, such as the piano, or listening to music can increase grey matter volume in areas such as thecaudate nucleus,Rolandic operculum, andcerebellum.[95] Evidence also suggests that music-supported therapy can improve cognitive performance, well-being, and social behavior in patients who are recovering from damage to theorbitofrontal cortex (OFC) and recovering from mild traumatic brain injury.Neuroimaging post music-supported therapy revealed functional changes in OFC networks, with improvements observed in both task-based and resting-statefMRI analyses.[96]
Aerobic exercise increases the production ofneurotrophic factors (compounds that promote growth or survival of neurons), such asbrain-derived neurotrophic factor (BDNF),insulin-like growth factor 1 (IGF-1), andvascular endothelial growth factor (VEGF).[97][98][99] Exercise-induced effects on the hippocampus are associated with measurable improvements inspatial memory.[100][101][102][103] Consistent aerobic exercise over a period of several months induces markedclinically significant improvements inexecutive function (i.e., the "cognitive control" of behavior) and increasedgray matter volume in multiple brain regions, particularly those that give rise to cognitive control.[99][100][104][105] The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are theprefrontal cortex andhippocampus;[99][100][101] moderate improvements are seen in theanterior cingulate cortex,parietal cortex,cerebellum,caudate nucleus, andnucleus accumbens.[99][100][101] Higherphysical fitness scores (measured byVO2 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.[100]
Due to hearing loss, theauditory cortex and other association areas of the brain in deaf and/or hard of hearing people undergo compensatory plasticity.[106][107][108] The auditory cortex usually reserved for processing auditory information in hearing people now is redirected to serve other functions, especially forvision andsomatosensation.
Deaf individuals have enhanced peripheral visual attention,[109] better motion change but not color change detection ability in visual tasks,[107][108][110] more effective visual search,[111] and faster response time for visual targets[112][113] compared to hearing individuals. Altered visual processing in deaf people is often found to be associated with the repurposing of other brain areas includingprimary auditory cortex,posterior parietal association cortex (PPAC), andanterior cingulate cortex (ACC).[114] A review by Bavelier et al. (2006) summarizes many aspects on the topic of visual ability comparison between deaf and hearing individuals.[115]
Brain areas that serve a function in auditory processing repurpose to process somatosensory information in congenitally deaf people. They have higher sensitivity in detecting frequency change in vibration above threshold[116] and higher and more widespread activation in auditory cortex under somatosensory stimulation.[117][106] However, speeded response for somatosensory stimuli is not found in deaf adults.[112]
Neuroplasticity is involved in the development of sensory function. The brain is born immature and then adapts to sensory inputs after birth. In the auditory system, congenital hearing loss, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of asensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system.[118] Due to a sensitive period for plasticity, there is also a sensitive period for such intervention within the first 2–4 years of life. Consequently, in prelingually deaf children, earlycochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.[119]
Due to vision loss, thevisual cortex in blind people may undergocross-modal plasticity, and therefore other senses may have enhanced abilities. Or the opposite could occur, with the lack of visual input weakening the development of other sensory systems. One study suggests that the right posterior middle temporal gyrus andsuperior occipital gyrus reveal more activation in the blind than in the sighted people during a sound-moving detection task.[120] Several studies support the latter idea and found weakened ability in audio distance evaluation, proprioceptive reproduction, threshold for visual bisection, and judging minimum audible angle.[121][122]
Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by someblind people to navigate their environment and sense their surroundings in detail. Studies in 2010[123] and 2011[124] usingfunctional magnetic resonance imaging techniques have shown that parts of the brain associated with visual processing are adapted for the new skill of echolocation. Studies with blind patients, for example, suggest that the click-echoes heard by these patients were processed by brain regions devoted to vision rather than audition.[124]
Reviews of MRI and electroencephalography (EEG) studies on individuals with ADHD suggest that the long-term treatment of ADHD with stimulants, such asamphetamine ormethylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the rightcaudate nucleus of thebasal ganglia,[125][126][127] leftventrolateral prefrontal cortex (VLPFC), andsuperior temporal gyrus.[128]
Neuroplasticity is most active in childhood as a part of normalhuman development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency.[129] Trauma is considered a great risk as it negatively affects many areas of the brain and puts a strain on thesympathetic nervous system from constant activation. Trauma thus alters the brain's connections such that children who have experienced trauma may be hyper vigilant or overly aroused.[130] However, a child's brain can cope with these adverse effects through the actions of neuroplasticity.[131]
Neuroplasticity is shown in four different categories in children and covering a wide variety of neuronal functioning. These four types include impaired, excessive, adaptive, and plasticity.[132]
There are many examples of neuroplasticity in human development. For example, Justine Ker and Stephen Nelson looked at the effects of musical training on neuroplasticity, and found that musical training can contribute to experience dependent structural plasticity. This is when changes in the brain occur based on experiences that are unique to an individual. Examples of this are learning multiple languages, playing a sport, doing theatre, etc. A study done by Hyde in 2009, showed that changes in the brain of children could be seen in as little as 15 months of musical training.[133] Ker and Nelson suggest this degree of plasticity in the brains of children can "help provide a form of intervention for children... with developmental disorders and neurological diseases."[134]
In a singlelifespan, individuals of an animalspecies may encounter various changes in brainmorphology. Many of these differences are caused by the release ofhormones in the brain; others are the product ofevolutionary factors ordevelopmental stages.[135][136][137][138] Some changes occur seasonally in species to enhance or generate response behaviors.
Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals.[139] These changes can improve the chances of mating during breeding season.[135][136][137][139][140][141] Examples of seasonal brain morphology change can be found within many classes and species.
Within the classAves, black-capped chickadees experience an increase in thevolume of theirhippocampus and strength of neural connections to the hippocampus during fall months.[142][143] These morphological changes within the hippocampus which are related tospatial memory are not limited to birds, as they can also be observed inrodents andamphibians.[139] Insongbirds, many song control nuclei in the brain increase in size during mating season.[139] Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common.[144]Gonadotropin-releasing hormone (GnRH)immunoreactivity, or the reception of the hormone, is lowered inEuropean starlings exposed to longer periods of light during the day.[135][136]
TheCalifornia sea hare, agastropod, has more successfulinhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain.[137] Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals.[138] In the amphibianBufo japonicus, part of theamygdala is larger before breeding and duringhibernation than it is after breeding.[140]
Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the commonewe is more receptive to GnRH during breeding season than at other times of the year.[141]Humans experience a change in the "size of the hypothalamicsuprachiasmatic nucleus andvasopressin-immunoreactive neurons within it"[138] during the fall, when these parts are larger. In the spring, both reduce in size.[145]
A group of scientists found that if a smallstroke (an infarction) is induced by obstruction of blood flow to a portion of a monkey's motor cortex, the part of the body that responds by movement moves when areas adjacent to the damaged brain area are stimulated. In one study, intracortical microstimulation (ICMS) mapping techniques were used in nine normal monkeys. Some underwent ischemic-infarction procedures and the others, ICMS procedures. The monkeys with ischemic infarctions retained more finger flexion during food retrieval and after several months this deficit returned to preoperative levels.[146] With respect to the distalforelimb representation, "postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex."[146] Understanding of interaction between the damaged and undamaged areas provides a basis for better treatment plans in stroke patients. Current research includes the tracking of changes that occur in the motor areas of the cerebral cortex as a result of a stroke. Thus, events that occur in the reorganization process of the brain can be ascertained. The treatment plans that may enhance recovery from strokes, such as physiotherapy,pharmacotherapy, and electrical-stimulation therapy, are also being studied.
Jon Kaas, a professor atVanderbilt University, has been able to show "how somatosensory area 3b and ventroposterior (VP) nucleus of the thalamus are affected by longstanding unilateral dorsal-column lesions at cervical levels in macaque monkeys."[147] Adult brains have the ability to change as a result of injury but the extent of the reorganization depends on the extent of the injury. His recent research focuses on the somatosensory system, which involves a sense of the body and its movements using many senses. Usually, damage of the somatosensory cortex results in impairment of the body perception. Kaas' research project is focused on how these systems (somatosensory, cognitive, motor systems) respond with plastic changes resulting from injury.[147]
One recent study of neuroplasticity involves work done by a team of doctors and researchers atEmory University, specificallyDonald Stein[148] and 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.[68] Stein noticed that female mice seemed to recover from brain injuries better than male mice, and that at certain points in theestrus 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 in human patients.[149]
Transcriptional profiling of thefrontal cortex of persons ranging from 26 to 106 years of age defined a set ofgenes with reduced expression after age 40, and especially after age 70.[150] Genes that play central roles insynaptic plasticity were the most significantly affected by age, generally showing reduced expression over time. There was also a marked increase in corticalDNA damage, likelyoxidative DNA damage, ingene promoters with aging.[150]
Reactive oxygen species appear to have a significant role in the regulation of synaptic plasticity and cognitive function.[151] However age-related increases in reactive oxygen species may also lead to impairments in these functions.
There is a beneficial effect of multilingualism on people's behavior and cognition. Numerous studies have shown that people who study more than one language have better cognitive functions and flexibilities than people who only speak one language. Bilinguals are found to have longer attention spans, stronger organization and analyzation skills, and a better theory of mind than monolinguals. Researchers have found that the effect of multilingualism on better cognition is due to neuroplasticity.[citation needed]
In one prominent study, neurolinguists used avoxel-based morphometry (VBM) method to visualize the structural plasticity of brains in healthy monolinguals and bilinguals. They first investigated the differences in density of grey and white matter between two groups and found the relationship between brain structure and age of language acquisition. The results showed that grey-matter density in the inferior parietal cortex for multilinguals were significantly greater than monolinguals. The researchers also found that early bilinguals had a greater density of grey matter relative to late bilinguals in the same region. The inferior parietal cortex is a brain region highly associated with the language learning, which corresponds to the VBM result of the study.[152]
Recent studies have also found that learning multiple languages not only re-structures the brain but also boosts brain's capacity for plasticity. A recent study found that multilingualism not only affects the grey matter but also white matter of the brain.White matter is made up of myelinated axons that is greatly associated with learning and communication. Neurolinguists used adiffusion tensor imaging (DTI) scanning method to determine the white matter intensity between monolinguals and bilinguals. Increased myelinations in white matter tracts were found in bilingual individuals who actively used both languages in everyday life. The demand of handling more than one language requires more efficient connectivity within the brain, which resulted in greater white matter density for multilinguals.[153]
While it is still debated whether these changes in brain are result of genetic disposition or environmental demands, many evidences suggest that environmental, social experience in early multilinguals affect the structural and functional reorganization in the brain.[154][155]
Historically, themonoamine imbalance hypothesis of depression played a dominant role in psychiatry and drug development.[156] However, while traditionalantidepressants cause a quick increase innoradrenaline,serotonin, ordopamine, there is a significant delay in their clinical effect and often an inadequate treatment response.[157] As neuroscientists pursued this avenue of research, clinical and preclinical data across multiple modalities began to converge on pathways involved in neuroplasticity.[158] They found a strong inverse relationship between the number ofsynapses and severity of depression symptoms[159] and discovered that in addition to theirneurotransmitter effect, traditional antidepressants improved neuroplasticity but over a significantly protracted time course of weeks or months.[160] The search for faster acting antidepressants found success in the pursuit ofketamine, a well-known anesthetic agent, that was found to have potent anti-depressant effects after a single infusion due to its capacity to rapidly increase the number of dendritic spines and to restore aspects of functional connectivity.[161] Additional neuroplasticity promoting compounds with therapeutic effects that were both rapid and enduring have been identified through classes of compounds includingserotonergic psychedelics,cholinergicscopolamine, and other novel compounds. To differentiate between traditional antidepressants focused on monoamine modulation and this new category of fast acting antidepressants that achieve therapeutic effects through neuroplasticity, the termpsychoplastogen was introduced.[162]
Exercise-related improvements in brain function and structure may be conferred by the concurrent adaptations in vascular function and structure. Aerobic exercise increases the peripheral levels of growth factors (e.g., BDNF, IFG-1, and VEGF) that cross the blood-brain barrier (BBB) and stimulate neurogenesis and angiogenesis (Trejo et al., 2001; Lee et al., 2002; Fabel et al., 2003; Lopez-Lopez et al., 2004).
Consistent evidence indicates that exercise improves cognition and mood, with preliminary evidence suggesting that brain-derived neurotrophic factor (BDNF) may mediate these effects. The aim of the current meta-analysis was to provide an estimate of the strength of the association between exercise and increased BDNF levels in humans across multiple exercise paradigms. We conducted a meta-analysis of 29 studies (N = 1111 participants) examining the effect of exercise on BDNF levels in three exercise paradigms: (1) a single session of exercise, (2) a session of exercise following a program of regular exercise, and (3) resting BDNF levels following a program of regular exercise. Moderators of this effect were also examined. Results demonstrated a moderate effect size for increases in BDNF following a single session of exercise (Hedges' g = 0.46, p < 0.001). Further, regular exercise intensified the effect of a session of exercise on BDNF levels (Hedges' g = 0.59, p = 0.02). Finally, results indicated a small effect of regular exercise on resting BDNF levels (Hedges' g = 0.27, p = 0.005). ... Effect size analysis supports the role of exercise as a strategy for enhancing BDNF activity in humans
Basal ganglia regions like the right globus pallidus, the right putamen, and the nucleus caudatus are structurally affected in children with ADHD. These changes and alterations in limbic regions like ACC and amygdala are more pronounced in non-treated populations and seem to diminish over time from child to adulthood. Treatment seems to have positive effects on brain structure.
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