neuroplasticity neuroplasticity neuroplasticity, also known as neural plasticity, or brain plasticity, is the ability of neural networks in the brain to change through growth and reorganization. it is when the brain is rewired to function in some way that differs from how it previously functioned. these changes range from individual neuron pathways making new connections, to systematic adjustments like cortical remapping. examples of neuroplasticity include circuit and network changes that result from learning a new ability, environmental influences, practice, and psychological stress. neuroplasticity was once thought by neuroscientists to manifest only during childhood, but 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. activity-dependent plasticity can have significant implications for healthy development, learning, memory, and recovery from brain damage. history origin the term plasticity was first applied to behavior in 1890 by william james in the 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". the first person to use the term neural plasticity appears to have been the polish neuroscientist jerzy konorski. one of the first experiments providing evidence for the neuroplasticity phenomenon was conducted in 1793 by italian anatomist michele vicenzo 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. in 1890, the idea that the brain and its function are not fixed throughout adulthood was proposed by william james in the principles of psychology, though the idea was largely neglected. up until the 1970s, neuroscientists believed that the brain's structure and function was essentially fixed throughout adulthood. while the brain was commonly understood as a nonrenewable organ in the early 1900s, santiago ramón y cajal, father of neuroscience, used the term neuronal plasticity to describe nonpathological changes in the structure of adult brains. based on his renowned neuron 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. he used the term plasticity in reference to his work on findings of degeneration and regeneration in the central nervous system after a person had reached adulthood, specifically. many neuroscientists used the term plasticity only to explain the regenerative capacity of the peripheral nervous system, which cajal's conceptual transfer of the term gave rise to a controversial discussion. 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. research and discovery in 1923, karl lashley conducted experiments on rhesus monkeys that demonstrated changes in neuronal pathways, which he concluded were evidence of plasticity. despite this, and other research that suggested plasticity took place, neuroscientists did not widely accept the idea of neuroplasticity. in 1945, justo gonzalo concluded from his research on 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 . 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. marian diamond of the university of california, berkeley, produced the first scientific evidence of anatomical brain plasticity, publishing her research in 1964. 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. 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 via sensory substitution. studies in people recovering from stroke 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. 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. 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." 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." neurobiology there are different ideas and theories on what biological process 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 via phosphorylation, the role of inflammation and inflammatory cytokines, proteins such as bcl-2 proteins and neutrophorins, and energy production via mitochondria. jt wall and j xu have traced the mechanisms underlying neuroplasticity. re-organization is not cortically emergent, but occurs at every level in the processing hierarchy; this produces the map changes observed in the cerebral cortex. types 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." correspondingly, two types of neuroplasticity are often discussed: structural neuroplasticity and functional neuroplasticity. structural neuroplasticity structural plasticity is often understood as the brain's ability to change its neuronal connections. new neurons are constantly produced and integrated into the central nervous system throughout the life span based on this type of neuroplasticity. 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. this type of neuroplasticity often studies the effect of various internal or external stimuli on the brain's anatomical reorganization. the changes of grey matter proportion or the synaptic strength in the brain are considered as examples of structural neuroplasticity. structural neuroplasticity is currently investigated more within the field of neuroscience in current academia. functional neuroplasticity functional plasticity refers to brain's ability to alter and adapt the functional properties of neurons. functional plasticity can occur in four known ways namely homologous area adaptation, map expansion, cross- model reassignment, and compensatory masquerade. through homologous area adaptation a cognitive task is shifted from a damaged part of the brain to its homologous area in the brain. functional changes like this 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. 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. the changes can occur in response to previous activity (activity-dependent plasticity) to acquire memory or in response to malfunction or damage of neurons (maladaptive plasticity) to compensate a pathological event. 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. regarding physiological forms of activity-dependent plasticity, those involving synapses are referred to as synaptic plasticity. the strengthening or weakening of synapses that results in an increase or decrease of firing rate of the neurons are called long-term potentiation (ltp) and long-term depression (ltd), respectively, and they are considered as examples of synaptic plasticity that are associated with memory. the cerebellum is a typical structure with combinations of ltp/ltd and redundancy within the circuitry, allowing plasticity at several sites. 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 as intrinsic plasticity.this, as opposed to homeostatic plasticity does not necessarily maintain the overall activity of a neuron within a network but contributes to encoding memories. also, many studies have indicated functional neuroplasticity in the level of brain networks, where training alters the strength of functional connections. 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. applications and examples the adult brain is not entirely "hard-wired" with fixed neuronal 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 for the active, experience-dependent re-organization of the synaptic networks of the brain involving multiple inter-related structures