127:. With conventional ideology being that the brain development is finalized upon adulthood, Bach y Rita designed several experiments in the late 1960s and 1970s that proved that the brain is capable of changing. These included a pivotal visual substitution method for blind people provided by tactile image projection in 1969. The basis behind this experiment was to take one sense and use it to detect another: in this case use the sense of touch on the tongue to visualize the surrounding. This experiment was years ahead of its time and led to many questions and applications. A similar experiment was reported again by Bach y Rita in 1986 where vibrotactile stimulation was delivered to the index fingertips of naive blindfolded subjects. Even though the experiment did not yield great results, it supported the study and proposed further investigations. In 1998, his design was even further developed and tested again with a 49-point electrotactile stimulus array on the tongue. He found that five sighted adult subjects recognized shapes across all sizes 79.8% of the time, a remarkable finding that has led to the incorporation of the tongue electrotactile stimulus into cosmetically acceptable and practical designs for blind people. In later years, he has published a number of other articles including "Seeing with the brain" in 2003 where Bach y Rita addresses the plasticity of the brain relative to visual learning. Here, images are enhanced and perceived by other plastic mechanisms within the realm of information passing to the brain.
599:
have suggested potential therapeutic approaches for a wide range of brain disorders in humans. Physiological and electrical stimulations as well as plasticity-modifying molecular agents may facilitate functional recovery by selectively enhancing existing neural circuits or promoting the formation of new functional circuits. ... Neural plasticity can be broadly defined as the ability of the nervous system to adopt a new functional or structural state in response to extrinsic and intrinsic factors. Such plasticity is essential for the development of the nervous system and normal functioning of the adult brain. Neural plasticity can manifest at the macroscale as changes in the spatiotemporal pattern of activation of different brain regions, at the mesoscale as alterations of long-range and local connections among distinct neuronal types, and at the microscale as modifications of neurons and synapses at the cellular and subcellular levels. Maladaptive neural plasticity may account for many developmental, acquired, and neurodegenerative brain disorders.
288:, a region of the brain that processes visual stimuli and is capable of modifying the experienced stimuli based on active sensing and arousal states. It is known that synaptic communication trends between excited and depressed states relative to the light/dark cycle. By experimentation on rats, it was found that visual experience during vigilant states leads to increased responsiveness and plastic changes in the visual cortex. More so, depressed states were found to negatively alter the stimulus so the reaction was not as energetic. This experiment proves that even the visual cortex is capable of achieving activity-dependent plasticity as it is reliant on both visual exploration and the arousal state of the animal.
393:, 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.
166:
476:, and adaptation are thought to involve LTP and LTD, two activity-dependent plasticity mechanisms that stress can directly suppress. Several experiments have been conducted in order to discover the specific mechanisms for this suppression and also possible intervention methods. Dr. Li and several others have actually identified the TRPV1 channel as a target to facilitate LTP and suppress LTD, therefore helping to protect the feature of synaptic plasticity and retention of memory from the effects of stress.
245:
459:. Dr. Gatto has found that early introduction of the product FMRP results in nearly complete restructuring of the synapses. This method is not as effective, though, when introduced into a mature subject and only partially accommodates for the losses of FMR1. The discovery of this gene provides a possible location for intervention for young children with these abnormalities as this gene and its product act early to construct synaptic architecture.
143:
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
58:'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
225:
more permanent changes and therefore result in plasticity. Hebb's postulate addresses this fact by stating that synaptic terminals are strengthened by correlated activity and will therefore sprout new branches. However, terminals that experience weakened and minimal activity will eventually lose their synaptic connection and deteriorate.
106:. 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
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A defining characteristic of the brain is its remarkable capacity to undergo activity-dependent functional and morphological remodeling via mechanisms of plasticity that form the basis of our capacity to encode and retain memories. Today, it is generally accepted that the neurobiological substrate of
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that left the 65-year-old man half-paralyzed and unable to speak. After one year of crawling and unusual therapy tactics including playing basic children's games and washing pots, his father's rehabilitation was nearly complete and he went back to his role as a professor at City
College in New York.
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In recent studies, a specific gene has also been identified as having a strong role in synapse growth and activity-dependent plasticity: the microRNA 132 gene (miR132). This gene is regulated by the cAMP response element-binding (CREB) protein pathway and is capable of enhancing dendritic growth when
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receptors are key molecules in mechanisms of long and short-term potentiation between neurons. NMDA receptors can detect local activity due to activation and therefore modify signaling in the post-synaptic cell. The increased activity and coordination between pre- and post-synaptic receptors leads to
85:
The brain's ability to adapt toward active functions allows humans to specialize in specific processes based on relative use and activity. For example, a right-handed person may perform any movement poorly with their left hand but continuous practice with the non-dominant hand can cause one to become
396:
Another research model of activity-dependent plasticity includes the excitatory corticostriatal pathway that is involved in information processing related to adaptive motor behaviors and displays long-lasting synaptic changes. The change in synaptic strength is responsible for motor learning and is
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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
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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
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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
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Much progress has been made in understanding how behavioral experience and neural activity can modify the structure and function of neural circuits during development and in the adult brain. Studies of physiological and molecular mechanisms underlying activity-dependent plasticity in animal models
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Since plasticity is such a fundamental property of brain function due to its involvement in brain development, brain repair, and cognitive processes, its proper regulation is necessary for normal physiology. Mutations within any of the genes associated with activity-dependent plasticity have been
296:
Activity-dependent plasticity plays a very important role in learning and in the ability of understanding new things. It is responsible for helping to adapt an individual's brain according to the relative amount of usage and functioning. In essence, it is the brain's ability to retain and develop
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Recent findings with both animals and humans suggest that decreases in microscopic movements of water in the hippocampus reflect short-term neuroplasticity resulting from learning. Here we examine whether such neuroplastic structural changes concurrently alter the functional connectivity between
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in activity-dependent transcription-related genes can lead to neurological disorders. Each of the studies' findings aims to help proper development of the brain while improving a wide variety of tasks such as speech, movement, comprehension, and memory. More so, the findings better explain the
484:
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
501:, 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.
419:. The two types of intellectual disability related to plasticity depend on dysfunctional neuronal development or alterations in molecular mechanisms involved in synaptic organization. Complications within either of these types can greatly reduce brain capability and
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Activity-dependent plasticity of one form or another has been observed in most areas of the brain. In particular, it is thought that the reorganization of sensory and motor maps involves a variety of pathways and cellular structures related to relative activity.
156:
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.
324:(IEG) that are rapidly transcribed in response to synaptic input. Of the estimated 30-40 genes that comprise the total neuronal IEG response, all are prototypical activity-dependent genes and a number have been implicated in learning and memory. For example,
232:
neurons. These receptors exist at postsynaptic sites and along with the regulation of local inhibitory synapses have been found to be very sensitive to critical period alterations. Any alteration to the receptors leads to changed concentrations of
248:
Illustration of the elements incorporated in synaptic transmission. An action potential is generated and travels down the axon to the axon terminal, where it is released and provokes a neurotransmitter release that acts on the post-synaptic
272:, which are receptors for extracellular matrix proteins and involved with CAMs, are explicitly incorporated in synapse maturation and memory formation. They play a crucial role in the feedback regulation of excitatory synaptic strength, or
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and also disorders associated with continuous stress. Many regions of the brain are very sensitive to stress and can be damaged with extended exposure. More importantly, many of the mechanisms involved with increased memory retention,
384:
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
1551:
French PJ, O'Connor V, Jones MW, Davis S, Errington ML, Voss K, Truchet B, Wotjak C, Stean T, et al. (2001). "Subfield-specific immediate early gene expression associated with hippocampal long-term potentiation in vivo".
280:
receptors, which result in quick, short synaptic currents. But, it is the metabotropic glutamate receptor 1 (mGlu1) that has been discovered to be required for activity-dependent synaptic plasticity in associative learning.
320:. The Arc gene is activity-regulated and the transcribed mRNA is localized to activated synaptic sites where the translated protein plays a role in AMPA receptor trafficking. Arc is a member of a class of proteins called
451:(FraX) is the result of this gene's loss of function. The FMR1 gene produces protein FMRP, which mediates activity-dependent control of synaptic structure. The loss or absence of this gene almost certainly leads to both
200:. 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 effect of the signal that fundamentally lead to the
134:, 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
257:
postsynaptic pathway, which is responsible for the coding and production of many molecules for development events, can be bidirectionally stimulated and is responsible for the downstream alteration of the
440:
This remarkable recovery from a stroke proves that even someone with abnormal behavior and severe medical complications can recover nearly all of the normal functions by much practice and perseverance.
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On the other hand, people with such conditions have the capacity to recover some degree of their lost abilities through continued challenges and use. An example of this can be seen in Norman Doidge's
1949:
Di
Filippo M, Sarchielli P, Picconi B, Calabresi P (2008). "Neuroinflammation and synaptic plasticity: theoretical basis for a novel, immune-centered, therapeutic approach to neurological disorders".
176:
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
180:. 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
652:
hippocampus and other regions involved in learning. ... These concurrent changes characterize the multidimensionality of neuroplasticity as it enables human spatial learning.
297:
memories based on activity-driven changes of synaptic strength that allow stronger learning of information. It is thought to be the growing and adapting quality of
918:
Kilgard MP, Pandya PK, Vazquez J, Gehi A, Schreiner CE, Merzenich MM (2001). "Sensory input directs spatial and temporal plasticity in primary auditory cortex".
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Calabresi P, Galletti F, Saggese E, Ghiglieri V, Picconi B (2007). "Neuronal networks and synaptic plasticity in
Parkinson's disease: beyond motor deficits".
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activated. The miR132 gene is another component that is responsible for the brain's plasticity and helps to establish stronger connections between neurons.
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dependent on the simultaneous activation of glutamatergic corticostriatal and dopaminergic nigrostriatal pathways. These are the same pathways affected in
309:. Dendritic spines accomplish this by transforming synaptic input into neuronal output and also by helping to define the relationship between synapses.
821:
Epstein W, Hughes B, Schneider S, Bach-y-Rita P (1986). "Is anything out there? A study of distal attribution in response to vibrotactile stimulation".
702:
memories resides in activity-driven modifications of synaptic strength and structural remodeling of neural networks activated during learning.
1072:
Purves, Dale; George J. Augustine; David
Fitzpatrick; William C. Hall; Anthony-Samuel LaMantia; James O. McNamara; Leonard E.r White (2008).
1047:
Purves, Dale; George J. Augustine; David
Fitzpatrick; William C. Hall; Anthony-Samuel LaMantia; James O. McNamara; Leonard E. White (2008).
1022:
Purves, Dale; George J. Augustine; David
Fitzpatrick; William C. Hall; Anthony-Samuel LaMantia; James O. McNamara; Leonard E. White (2008).
1238:"Intrinsic, light-independent and visual activity-dependent mechanisms cooperate in the shaping of the field response in rat visual cortex"
1373:"Arc, a growth factor and activity-regulated gene, encodes a novel cytoskeletal-associated protein that is enriched in neuronal dendrites"
864:
Bach-y-Rita P, Kaczmarek K, Tyler M, Garcia-Lara J (1998). "Form perception with a 49-point electrotactile stimulus array on the tongue".
1656:"Brain-derived neurotrophic factor-tropomyosin-related kinase B signaling contributes to activity-dependent changes in synaptic proteins"
262:
neuron. When the Wg presynaptic pathway is activated, however, it alters cytoskeletal structure through transcription and translation.
497:. In addition to a better understanding of the various disorders, neurologists should and will look at the plasticity incurred by the
1707:"Synaptic function for the Nogo-66 receptor NgR1: Regulation of dendritic spine morphology and activity-dependent synaptic strength"
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in the affected cells and can ultimately influence dendritic and axonal branching. This concentration change is the result of many
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which carry the output information to other neurons. The dendrites and axons are interfaced through a small connection called a
1906:
Li HB, Mao RR, Zhang JC, Cao YJ, Xu L (2008). "Antistress effect of TRPV1 channel on synaptic plasticity and spatial memory".
1841:
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1056:
1031:
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Chowdhury S, Shepherd JD, Okuno H, Lyford G, Petralia RS, Plath N, Kuhl D, Huganir RL, Worley PF, et al. (2006).
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plasticity would help treat and perhaps cure. These include autism, different severities of intellectual disability,
401:, and the degeneration of synapses within this disorder may be responsible for the loss of some cognitive abilities.
386:
268:(CAMs) are also important in plasticity as they help coordinate the signaling across the synapse. More specifically,
188:, which is equipped with dendritic branches that mostly receive the incoming inputs from other neurons; a long, thin
770:
Bach-y-Rita P, Collins CC, Sauders F, White B, Scadden L (1969). "Vision substitution by tactile image projection".
254:
1197:"Involvement of the mGluR1 receptor in hippocampal synaptic plasticity and associative learning in behaving mice"
667:
Bruel-Jungerman E, Davis S, Laroche S (October 2007). "Brain plasticity mechanisms and memory: a party of four".
1099:"Rapid Activity-Dependent Modifications in Synaptic Structure and Function Require Bidirectional Wnt Signaling"
1285:
Sala C, Cambianica I, Rossi F (2008). "Molecular mechanisms of dendritic spine development and maintenance".
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Figure 3: Calcium-induced signal transduction networks mediating neuronal activity-dependent gene expression.
1859:"Temporal Requirements of the Fragile X Mental Retardation Protein in the Regulation of Synaptic Structure"
333:
139:
79:
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1414:"Differential intracellular sorting of immediate early gene mRNAs depends on signals in the mRNA sequence"
1463:"Selective targeting of newly synthesized Arc mRNA to active synapses requires NMDA receptor activation"
716:"Signaling mechanisms linking neuronal activity to gene expression and plasticity of the nervous system"
1989:
1148:"Activity-Dependent Regulation of Synaptic AMPA Receptor Composition and Abundance by β3 Integrins"
369:
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456:
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153:
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There are a variety of mechanisms involved in activity-dependent plasticity. These include LTP,
974:"Cross-modal extinction in a boy with severely autistic behaviour and high verbal intelligence"
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The Brain That
Changes Itself: Stories of personal triumph from the frontiers of brain science
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Lyford GL, Yamagata K, Kaufmann WE, Barnes CA, Sanders LK, Copeland NG, Worley PF (1995).
8:
1314:"An activity-regulated microRNA controls dendritic plasticity by down-regulating p250GAP"
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influx, which in turn trigger cellular changes that affect synaptic connections and gene
364:. The mechanisms of activity-dependent plasticity result in membrane depolarization and
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Vaillend C, Poirier R, Laroche S (2008). "Genes, plasticity and mental retardation".
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1504:"Arc Interacts with the Endocytic Machinery to Regulate AMPA Receptor Trafficking"
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A major target of all molecular signaling is the inhibitory connections made by
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Proceedings of the
National Academy of Sciences of the United States of America
613:"Structural and functional neuroplasticity in human learning of spatial routes"
526:
361:
185:
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1597:"Synapse elimination accompanies functional plasticity in hippocampal neurons"
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being activated, the byproduct of which may enhance specific gene expression.
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activity, as opposed to forms of neuroplasticity that arise from extrinsic or
38:. Activity-dependent plasticity is a form of neuroplasticity that arises from
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A common issue amongst most people in the United States is high levels of
389:(BDNF), an activity-dependent synapse-development protein. In addition to
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Bach-y-Rita P, Tyler ME, Kaczmarek KA (2003). "Seeing with the brain".
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Many molecules have been implicated in synaptic plasticity. Notably,
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Diagram displaying components of a myelinated vertebrate motorneuron.
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Another pioneer within the field of activity-dependent plasticity is
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Another plasticity-related gene involved in learning and memory is
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Bastrikova N, Gardner GA, Reece JM, Jeromin A, Dudek SM (2008).
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The idea of neural plasticity was first proposed during 1890 by
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and personal experience; hence, it is the biological basis for
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1076:. Sunderland, MA: Sinauer Associates, Inc. pp. 630–32.
1051:. Sunderland, MA: Sinauer Associates, Inc. pp. 625–26.
568:"Activity-dependent neural plasticity from bench to bedside"
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that provide the basis for synaptic plasticity connected to
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276:(LTP), and help to control synaptic strength by regulating
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Gil-Sanz C, Delgado-Garcia JM, Fairen A, Gruart A (2008).
1026:. Sunderland, MA: Sinauer Associates, Inc. pp. 3–11.
960:
447:, is highly involved in activity-dependent plasticity and
16:
Neuroplasticity that arise from use of cognitive functions
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that contains genetic information; the cell body, or the
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The history of activity-dependent plasticity begins with
82:, among many others) during increased neuronal activity.
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related to dendritic branching and synapse development.
1788:
415:
found to positively correlate with various degrees of
1412:
Wallace CS, Lyford GL, Worley PF, Steward O (1998).
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344:(LTP), a cellular correlate of learning and memory.
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International
Journal of Human-Computer Interaction
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443:Recent studies have reported that a specific gene,
1981:
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138:. While assessing the recorded changes in the
1905:
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284:Activity-dependent plasticity is seen in the
253:In addition, it has been identified that the
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1836:. New York: Penguin Group. pp. 20–24.
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372:. In essence, neuronal activity regulates
208:Structures and molecular pathways involved
110:. It was believed that each region of the
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119:Pioneers of activity-dependent plasticity
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435:. Bach y Rita's father had a disabling
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243:
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54:- or drug-induced neuroplasticity. The
22:is a form of functional and structural
1982:
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732:10.1146/annurev.neuro.31.060407.125631
347:
1653:
1756:Parkinsonism & Related Disorders
1236:Tsanov M, Manahan-Vaughn D (2007).
611:Keller TA, Just MA (January 2016).
381:development induced by plasticity.
291:
13:
1951:Trends in Pharmacological Sciences
1430:10.1523/JNEUROSCI.18-01-00026.1998
1146:Cingolani LA; et al. (2007).
566:Ganguly K, Poo MM (October 2013).
14:
2001:
714:Flavell SW, Greenberg ME (2008).
542:Spike-timing-dependent plasticity
479:
387:brain-derived neurotrophic factor
1566:10.1046/j.0953-816x.2001.01467.x
630:10.1016/j.neuroimage.2015.10.015
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1312:Wayman GA; et al. (2008).
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972:Bonneh YS; et al. (2008).
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148:specific complications such as
1920:10.1016/j.biopsych.2008.02.020
1723:10.1523/jneurosci.5586-07.2008
1254:10.1523/jneurosci.1180-07.2007
1097:Ataman B; et al. (2008).
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66:that are activated by various
1:
1768:10.1016/S1353-8020(08)70013-0
1480:10.1016/S0896-6273(01)00275-6
1461:Steward O, Worley PF (2001).
548:
433:The Brain That Changes Itself
356:(LTD), synaptic elimination,
20:Activity-dependent plasticity
1857:Gatto CL, Broadie K (2008).
1705:Lee HJ; et al. (2008).
1520:10.1016/j.neuron.2006.08.033
1390:10.1016/0896-6273(95)90299-6
1164:10.1016/j.neuron.2008.04.011
1115:10.1016/j.neuron.2008.01.026
585:10.1016/j.neuron.2013.10.028
340:have all been implicated in
140:primary somatosensory cortex
52:electrical brain stimulation
26:that arises from the use of
7:
1654:Jia J; et al. (2008).
897:10.1207/s15327590ijhc1502_6
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10:
2006:
1963:10.1016/j.tips.2008.06.005
1601:Proc. Natl. Acad. Sci. USA
920:Journal of Neurophysiology
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1803:10.1016/j.bbr.2008.01.009
993:10.1080/02643290802106415
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34:and the formation of new
932:10.1152/jn.2001.86.1.326
681:10.1177/1073858407302725
405:Relationship to behavior
104:Principles of Psychology
1832:Doidge, Norman (2007).
1622:10.1073/pnas.0800027105
1339:10.1073/pnas.0803072105
457:intellectual disability
417:intellectual disability
410:Intellectual disability
266:Cell adhesion molecules
154:intellectual disability
62:which are triggered by
1673:10.1074/jbc.M800282200
512:Central nervous system
342:long-term potentiation
274:long-term potentiation
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170:
1908:Biological Psychiatry
1214:10.1093/cercor/bhm193
427:Stroke rehabilitation
322:immediate early genes
286:primary visual cortex
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1074:Neuroscience, 4th Ed
1049:Neuroscience, 4th Ed
1024:Neuroscience, 4th Ed
961:Fast ForWord Website
866:Rehab Research Devel
537:Sensory substitution
354:long-term depression
161:Structure of neurons
1613:2008PNAS..105.3123B
1330:2008PNAS..105.9093W
1287:Acta Neurobiol. Exp
784:1969Natur.221..963B
720:Annu. Rev. Neurosci
491:Parkinson's disease
399:Parkinson's disease
348:Mechanisms involved
68:signaling molecules
28:cognitive functions
1875:10.1242/dev.022244
449:fragile X syndrome
251:
171:
64:signaling cascades
1843:978-0-14-311310-2
1083:978-0-87893-697-7
1058:978-0-87893-697-7
1033:978-0-87893-697-7
981:Cogn Neuropsychol
132:Michael Merzenich
50:factors, such as
1997:
1975:
1974:
1946:
1940:
1939:
1903:
1897:
1896:
1886:
1854:
1848:
1847:
1829:
1823:
1822:
1791:Behav. Brain Res
1786:
1780:
1779:
1751:
1745:
1744:
1734:
1702:
1696:
1695:
1685:
1675:
1666:(30): 21242–50.
1651:
1645:
1644:
1634:
1624:
1592:
1586:
1585:
1548:
1542:
1541:
1531:
1499:
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1458:
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1392:
1368:
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1341:
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1282:
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1233:
1227:
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1192:
1186:
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1175:
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1126:
1094:
1088:
1087:
1069:
1063:
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1044:
1038:
1037:
1019:
1013:
1012:
978:
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958:
952:
951:
915:
909:
908:
880:
874:
873:
861:
855:
854:
818:
812:
811:
792:10.1038/221963a0
778:(5184): 963–64.
767:
761:
753:
743:
711:
705:
704:
664:
655:
654:
632:
608:
602:
601:
587:
563:
517:Chemical synapse
332:, beta-activin,
299:dendritic spines
292:Role in learning
125:Paul Bach y Rita
2005:
2004:
2000:
1999:
1998:
1996:
1995:
1994:
1990:Neuroplasticity
1980:
1979:
1978:
1947:
1943:
1904:
1900:
1869:(15): 2637–48.
1855:
1851:
1844:
1830:
1826:
1787:
1783:
1752:
1748:
1717:(11): 2753–65.
1703:
1699:
1652:
1648:
1593:
1589:
1549:
1545:
1500:
1496:
1459:
1455:
1410:
1406:
1369:
1365:
1324:(26): 9093–98.
1310:
1306:
1283:
1279:
1248:(31): 8422–29.
1234:
1230:
1201:Cerebral Cortex
1193:
1189:
1144:
1140:
1095:
1091:
1084:
1070:
1066:
1059:
1045:
1041:
1034:
1020:
1016:
976:
970:
966:
959:
955:
916:
912:
881:
877:
862:
858:
835:10.1068/p150275
819:
815:
768:
764:
712:
708:
665:
658:
609:
605:
564:
555:
551:
546:
532:Neuroplasticity
522:Dendritic spine
507:
482:
465:
429:
412:
407:
374:gene expression
350:
294:
210:
163:
121:
108:critical period
96:
60:gene expression
24:neuroplasticity
17:
12:
11:
5:
2003:
1993:
1992:
1977:
1976:
1941:
1898:
1849:
1842:
1824:
1781:
1746:
1697:
1646:
1607:(8): 3123–27.
1587:
1560:(5): 968–976.
1554:Eur J Neurosci
1543:
1514:(3): 445–459.
1494:
1473:(1): 227–240.
1453:
1404:
1383:(2): 433–445.
1363:
1304:
1293:(2): 289–304.
1277:
1228:
1207:(7): 1653–63.
1187:
1138:
1089:
1082:
1064:
1057:
1039:
1032:
1014:
964:
953:
910:
875:
856:
813:
762:
760:
759:
706:
675:(5): 492–505.
669:Neuroscientist
656:
603:
578:(3): 729–741.
552:
550:
547:
545:
544:
539:
534:
529:
527:Hebbian theory
524:
519:
514:
508:
506:
503:
493:, stress, and
481:
480:Future studies
478:
464:
461:
428:
425:
411:
408:
406:
403:
362:synaptogenesis
349:
346:
293:
290:
209:
206:
194:axon terminals
162:
159:
120:
117:
95:
92:
15:
9:
6:
4:
3:
2:
2002:
1991:
1988:
1987:
1985:
1972:
1968:
1964:
1960:
1957:(8): 402–12.
1956:
1952:
1945:
1937:
1933:
1929:
1925:
1921:
1917:
1914:(4): 286–92.
1913:
1909:
1902:
1894:
1890:
1885:
1880:
1876:
1872:
1868:
1864:
1860:
1853:
1845:
1839:
1835:
1828:
1820:
1816:
1812:
1808:
1804:
1800:
1797:(1): 88–105.
1796:
1792:
1785:
1777:
1773:
1769:
1765:
1762:: S259–S262.
1761:
1757:
1750:
1742:
1738:
1733:
1728:
1724:
1720:
1716:
1712:
1708:
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1660:J. Biol. Chem
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1210:
1206:
1202:
1198:
1191:
1183:
1179:
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1169:
1165:
1161:
1158:(5): 749–62.
1157:
1153:
1149:
1142:
1134:
1130:
1125:
1120:
1116:
1112:
1109:(5): 705–18.
1108:
1104:
1100:
1093:
1085:
1079:
1075:
1068:
1060:
1054:
1050:
1043:
1035:
1029:
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1018:
1010:
1006:
1002:
998:
994:
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987:(5): 635–52.
986:
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968:
962:
957:
949:
945:
941:
937:
933:
929:
926:(1): 326–38.
925:
921:
914:
906:
902:
898:
894:
891:(2): 285–95.
890:
886:
879:
871:
867:
860:
852:
848:
844:
840:
836:
832:
829:(3): 275–84.
828:
824:
817:
809:
805:
801:
797:
793:
789:
785:
781:
777:
773:
766:
758:
755:
754:
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747:
742:
737:
733:
729:
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721:
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698:
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686:
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581:
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569:
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523:
520:
518:
515:
513:
510:
509:
502:
500:
499:immune system
496:
492:
488:
487:schizophrenia
477:
475:
474:comprehension
470:
460:
458:
454:
450:
446:
441:
438:
434:
424:
422:
421:comprehension
418:
402:
400:
394:
392:
388:
382:
379:
375:
371:
370:transcription
367:
363:
359:
355:
345:
343:
339:
336:, Homer, and
335:
331:
327:
323:
319:
314:
310:
308:
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289:
287:
282:
279:
275:
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267:
263:
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256:
246:
242:
240:
236:
231:
226:
223:
219:
214:
205:
203:
199:
195:
191:
187:
183:
179:
178:motor neurons
175:
167:
158:
155:
151:
146:
141:
137:
133:
128:
126:
116:
113:
109:
105:
101:
100:William James
91:
89:
83:
81:
77:
73:
69:
65:
61:
57:
53:
49:
45:
41:
37:
33:
29:
25:
21:
1954:
1950:
1944:
1911:
1907:
1901:
1866:
1862:
1852:
1833:
1827:
1794:
1790:
1784:
1759:
1755:
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1714:
1710:
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1649:
1604:
1600:
1590:
1557:
1553:
1546:
1511:
1507:
1497:
1470:
1466:
1456:
1424:(1): 26–35.
1421:
1417:
1407:
1380:
1376:
1366:
1321:
1317:
1307:
1290:
1286:
1280:
1245:
1241:
1231:
1204:
1200:
1190:
1155:
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1092:
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967:
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884:
878:
869:
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859:
826:
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816:
775:
771:
765:
723:
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700:
672:
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650:
620:
616:
606:
597:
575:
571:
483:
466:
442:
432:
430:
413:
395:
383:
358:neurogenesis
351:
315:
311:
295:
283:
264:
260:postsynaptic
252:
227:
215:
211:
172:
145:Fast ForWord
129:
122:
103:
97:
88:ambidextrous
84:
19:
18:
1863:Development
1711:J. Neurosci
1242:J. Neurosci
623:: 256–266.
192:that bears
1418:J Neurosci
823:Perception
726:: 563–90.
617:NeuroImage
549:References
318:Arc/Arg3.1
202:plasticity
136:plasticity
44:endogenous
872:: 427–30.
378:Mutations
270:integrins
230:GABAergic
204:feature.
80:glutamate
48:exogenous
40:intrinsic
1984:Category
1971:18617277
1936:23943283
1928:18405883
1893:18579676
1819:19883660
1811:18329113
1776:18267247
1741:18337405
1692:18474605
1641:18287055
1582:38975364
1574:11264669
1538:17088211
1489:11343657
1358:18577589
1299:18511962
1272:17670989
1223:18024992
1182:18549786
1133:18341991
1009:14923473
1001:18651259
940:11431514
750:18558867
689:17901258
639:26477660
594:24183023
505:See also
303:learning
76:dopamine
36:memories
32:learning
1884:2753511
1732:6670664
1683:3258936
1632:2268595
1609:Bibcode
1529:1784006
1448:9412483
1439:6793378
1399:7857651
1349:2449370
1326:Bibcode
1263:6673071
1173:2446609
1124:2435264
948:6777933
851:2473076
843:3797201
808:4179427
800:5818337
780:Bibcode
741:2728073
697:2203266
647:2784354
366:calcium
239:kinases
235:calcium
198:synapse
182:nucleus
174:Neurons
94:History
72:calcium
70:(e.g.,
1969:
1934:
1926:
1891:
1881:
1840:
1817:
1809:
1774:
1739:
1729:
1690:
1680:
1639:
1629:
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1508:Neuron
1487:
1467:Neuron
1446:
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1377:Neuron
1356:
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1297:
1270:
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1152:Neuron
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1103:Neuron
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772:Nature
748:
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645:
637:
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572:Neuron
495:stroke
469:stress
463:Stress
453:autism
437:stroke
360:, and
326:zif268
307:memory
150:autism
78:, and
1932:S2CID
1815:S2CID
1578:S2CID
1005:S2CID
977:(PDF)
944:S2CID
901:S2CID
847:S2CID
804:S2CID
693:S2CID
643:S2CID
338:COX-2
112:brain
56:brain
1967:PMID
1924:PMID
1889:PMID
1838:ISBN
1807:PMID
1772:PMID
1737:PMID
1688:PMID
1637:PMID
1570:PMID
1534:PMID
1485:PMID
1444:PMID
1395:PMID
1354:PMID
1295:PMID
1268:PMID
1219:PMID
1178:PMID
1129:PMID
1078:ISBN
1053:ISBN
1028:ISBN
997:PMID
936:PMID
839:PMID
796:PMID
746:PMID
685:PMID
635:PMID
590:PMID
455:and
445:FMR1
391:BDNF
305:and
278:AMPA
249:end.
222:NMDA
220:and
218:AMPA
190:axon
186:soma
152:and
115:on.
1959:doi
1916:doi
1879:PMC
1871:doi
1867:135
1799:doi
1795:192
1764:doi
1727:PMC
1719:doi
1678:PMC
1668:doi
1664:283
1627:PMC
1617:doi
1605:105
1562:doi
1524:PMC
1516:doi
1475:doi
1434:PMC
1426:doi
1385:doi
1344:PMC
1334:doi
1322:105
1258:PMC
1250:doi
1209:doi
1168:PMC
1160:doi
1119:PMC
1111:doi
989:doi
928:doi
893:doi
831:doi
788:doi
776:221
736:PMC
728:doi
677:doi
625:doi
621:125
580:doi
334:tPA
330:Arc
102:in
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42:or
1986::
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1930:.
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Text is available under the Creative Commons Attribution-ShareAlike License. Additional terms may apply.
