Пластичность мозга: возможности к изменениям и адаптации

Ability of the brain to continuously change

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 or neural oscillation. Other forms of neuroplasticity include homologous area adaptation, cross modal reassignment, map expansion, and compensatory masquerade. Examples of neuroplasticity include circuit and network changes that result from learning a new ability, information acquisition, caloric intake, 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. Activity dependent plasticity can have significant implications for healthy development, learning, memory, and recovery from brain damage.

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. 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. 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. 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.

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 including the cerebral cortex. The specific details of how this process occurs at the molecular and ultrastructural 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 and neural 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 of classical conditioning in invertebrate animal models such as Aplysia. There is evidence that neurogenesis (birth of brain cells) occurs in the adult, rodent brain—and such changes can persist well into old age. The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but research has revealed that other parts of the brain, including the cerebellum, may be involved as well.

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 of acquired brain injury with goal directed experiential therapeutic programs in the context of rehabilitation 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 include constraint induced movement therapy, functional electrical stimulation, treadmill training with body weight support, and virtual 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. One group has developed a treatment that includes increased levels of progesterone injections in brain injured patients. "Administration of progesterone after traumatic brain injury (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory motor recovery." In a clinical trial, a group of severely injured patients had a 60% reduction in mortality after three days of progesterone injections.

For decades, researchers assumed that humans had to acquire binocular vision, in particular stereopsis, in early childhood or they would never gain it. In recent years, however, successful improvements in persons with amblyopia, convergence insufficiency or other stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.

In the phenomenon of phantom limb sensation, a person continues to feel pain or sensation within a part of their body that has been amputated. This is strangely common, occurring in 60–80% of amputees. An explanation for this is based on the concept of neuroplasticity, as the cortical maps of the removed limbs are believed to have become engaged with the area around them in the postcentral gyrus. This results in activity within the surrounding area of the cortex being misinterpreted by the area of the cortex formerly responsible for the amputated limb. The relationship between phantom limb sensation and neuroplasticity is a complex one. In the early 1990s V. S. Ramachandran theorized that phantom limbs were the result of cortical remapping. However, in 1995 Herta Flor and her colleagues demonstrated that cortical remapping occurs only in patients who have phantom pain. Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization. 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 configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body. The authors stated that: "In fact, this finding extends our understanding of the brain's plasticity because it is evidence that profound changes in the mental representation of the body can be induced purely by internal brain mechanisms—the brain truly does change itself."

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 and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization. For instance, individuals experiencing complex regional pain syndrome demonstrate a diminished cortical somatotopic representation of the hand contralaterally as well as a decreased spacing between the hand and the mouth. Additionally, chronic pain has been reported to significantly reduce the volume of grey matter in the brain globally, and more specifically at the prefrontal cortex and right thalamus. However, following treatment, these abnormalities in cortical reorganization and grey matter volume are resolved, as well as their symptoms. Similar results have been reported for phantom limb pain, chronic low back pain and carpal tunnel syndrome.

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter. One of the most well known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000. Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in collaboration with the Dalai 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 with attention, anxiety, depression, fear, anger, and compassion as well as the ability of the body to heal itself.

There is substantial evidence that artistic engagement in a therapeutic environment can create changes in neural network connections as well as increase cognitive flexibility. 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". 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 at VAGA, has written that "evolutionary theory links the symbolic nature of art to critical pivotal brain changes in Homo sapiens supporting increased development of language and hierarchical social grouping".

Aerobic exercise increases the production of neurotrophic factors (compounds that promote growth or survival of neurons), such as brain derived neurotrophic factor (BDNF), insulin like growth factor 1 (IGF 1), and vascular endothelial growth factor (VEGF). Consistent aerobic exercise over a period of several months induces marked clinically significant improvements in executive function (i. e., the "cognitive control" of behavior) and increased gray matter volume in multiple brain regions, particularly those that give rise to cognitive control. The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus; The auditory cortex is usually reserved for processing auditory information in hearing people now is redirected to serve other functions, especially for vision and somatosensation. Deaf individuals have enhanced peripheral visual attention, better motion change but not color change detection ability in visual tasks, more effective visual search, and faster response time for visual targets compared to hearing individuals. Altered visual processing in deaf people is often found to be associated with the repurposing of other brain areas including primary auditory cortex, posterior parietal association cortex (PPAC), and anterior cingulate cortex (ACC). A review by Bavelier et al. (2006) summarizes many aspects on the topic of visual ability comparison between deaf and hearing individuals. 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 and higher and more widespread activation in auditory cortex under somatosensory stimulation. 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, early cochlear implantation, as a rule, allows the children to learn the mother language and acquire acoustic communication.

Due to vision loss, the visual cortex in blind people may undergo cross 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 and superior occipital gyrus reveal more activation in the blind than in the sighted people during a sound moving detection task. 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.

Human echolocation is a learned ability for humans to sense their environment from echoes. This ability is used by some blind people to navigate their environment and sense their surroundings in detail. Studies in 2010 and 2011 left ventrolateral prefrontal cortex (VLPFC), and superior temporal gyrus.

Neuroplasticity is most active in childhood as a part of normal human development, and can also be seen as an especially important mechanism for children in terms of risk and resiliency. Trauma is considered a great risk as it negatively affects many areas of the brain and puts a strain on the sympathetic 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. However, a child's brain can cope with these adverse effects through the actions of neuroplasticity. 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. 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. 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."

In a single lifespan, individuals of an animal species may encounter various changes in brain morphology. Many of these differences are caused by the release of hormones in the brain; others are the product of evolutionary factors or developmental stages. These morphological changes within the hippocampus which are related to spatial memory are not limited to birds, as they can also be observed in rodents and amphibians. Gonadotropin releasing hormone (GnRH) immunoreactivity, or the reception of the hormone, is lowered in European starlings exposed to longer periods of light during the day.

Randy Nudo's group found that if a small stroke (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. 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.

Transcriptional profiling of the frontal cortex of persons ranging from 26 to 106 years of age defined a set of genes with reduced expression after age 40, and especially after age 70. However age related increases in reactive oxygen species may also lead to impairments in these functions.

The beneficial effect of multilingualism on people's behavior and cognition is well known nowadays. 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. In one prominent study, neurolinguists used a voxel 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. 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 a diffusion 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. 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.

Historically, the monoamine imbalance hypothesis of depression played a dominant role in psychiatry and drug development. However, while traditional antidepressants cause a quick increase in noradrenaline, serotonin, or dopamine, there is a significant delay in their clinical effect and often an inadequate treatment response. As neuroscientists pursued this avenue of research, clinical and preclinical data across multiple modalities began to converge on pathways involved in neuroplasticity. They found a strong inverse relationship between the number of synapses and severity of depression symptoms and discovered that in addition to their neurotransmitter effect, traditional antidepressants improved neuroplasticity but over a significantly protracted time course of weeks or months. The search for faster acting antidepressants found success in the pursuit of ketamine, 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. Additional neuroplasticity promoting compounds with therapeutic effects that were both rapid and enduring have been identified through classes of compounds including serotonergic psychedelics, cholinergic scopolamine, 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 term psychoplastogen was introduced.