Khác biệt giữa bản sửa đổi của “Khả biến thần kinh”

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Phiên bản lúc 08:42, ngày 7 tháng 9 năm 2016

Trái ngược với suy nghĩ thông thường như được thể hiện trong sơ đồ này, các chức năng của não không bị giới hạn trong nhưng vị trí cố định.

Tính khả biến thần kinh (tiếng Anh: Neuroplasticity) là một thuật ngữ ô mô tả sự thay đổi bền vững của não bộ trong suốt cuộc đời của một cá nhân. Khái niệm này phổ biến vào nửa cuối thế kỷ 20 khi những nghiên cứu mới[1] cho thấy nhiều khía cạnh của não vẫn có thể thay đổi được (hay "khả biến") thậm chí sau khi trưởng thành.[2] Khái niệm này trái ngược với nhận thức khoa học chung rằng não phát triển trong giai đoạn quan trọng ở trẻ nhỏ, sau đó tương đối không thay đổi được (hay "bất biến").[3]

Biến đổi thần kinh có thể xảy ra ở quy mô nhỏ, ví dụ như thay đổi vật lý đối với từng nơ-ron, hay ở quy mô toàn-não, như tái ánh xạ vỏ não sau chấn thuơng; tuy nhiên tái ánh xạ vỏ não chỉ xảy ra trong một khoảng thời gian nhất định -- nếu một đứa trẻ bị chấn thương não thì tái ánh xạ vỏ não có khả năng cao xảy ra còn với người lớn, nó không xảy ra vì bộ não đã hoàn thành hầu hết các kết nối của nó.[4] Hành vi, tác nhân môi trường, suy nghĩ và cảm xúc cũng có thể gây ra thay đổi, điều có ngụ ý quan trọng đối với sự phát triển lành mạnh của não, việc học, ghi nhớ, và phục hồi chấn thương não.[4][5][6]

Các nhà thần kinh học phân biệt biến đổi xi-náp, thay đổi trong cách các nơ-ron kết nối với nhau, và biến đổi phi xi-náp, biến đổi trong bản thân nơ-ron.

Thuyết định vị

Suốt từ cuối thế kỷ 16, nghiên cứu thần kinh học đã sử dụng mô thức của thuyết định vị, cái nói rằng não người hoạt động thông qua các cấu phần được phân công một chức năng duy nhất, như là nền tảng cho mọi nghiên cứu. Trước thuyết định vị, người Hy Lạp đưa ra một mô thức nguyên sơ hơn: ý tưởng rằng toàn vũ trụ hoạt động như một sinh thể, dẫn đến các cơ quan trong cơ thể người được coi không hơn những vật thể vô sinh mệnh. Niềm tin này bắt nguồn từ sự hoà quyện tư duy luận lý với tư duy thường nhật và tôn giáo.[7] Kỹ thuật thời đó cũng còn rất thô sơ không cho phép tìm ra vấn đề của các lý thuyết và phương pháp cũ.

Khi thuyết định vị khởi phát, sự đối lập với những thuyết trước đó kêu gọi một cuộc cải tổ hoàn toàn các lý thuyết thần kinh và dẫn đến sự bùng nổ khám phá khoa học, phóng nghiên cứu thần kinh học vào thời hiện đại. Nhà thiên văn nổi tiếng Galileo Galilei được gắn công sáng tạo ra thuyết định vị. Theo Norman Doidge, những nghiên cứu về vũ trụ và các thiên thể khiến Galileo tin rằng "toàn bộ tự nhiên hoạt động như một chiếc đồng hồ lớn" và những thiên thể này "bắt đầu giải thích những cá thể sinh vật, bao gồm cả các cơ quan, một cách cơ học".[8] Khi áp dụng vào não bộ, điều này có nghĩa những cấu phần của nó có chức năng cố định giống như một cỗ máy các các cấu phần được đặt vào vị trí nhất đinh. Theo thuyết này, không thể sửa một cấu phần bị hư hỏng. Các bác sỹ do đó coi một số bệnh hoặc hội chứng là không thể chữa được.

Sinh học thần kinh

Một nguyên lý cơ bản của tính khả biến thần kinh liên quan đến khái niệm cắt tỉa xi-náp, ý tưởng rằng các kết nối cá biệt trong não được liên tục loại bỏ hay tái tạo, chủ yếu tuỳ theo chúng được dùng ra sao.

Bản đồ vỏ não

Tổ chức vỏ não, đặc biệt với hệ thống cảm giác, thường được mô tả bằng khái niệm bản đồ.[9] Ví dụ, thông tin cảm giác từ chân phóng chiếu đến một vùng vỏ não và từ tay đến một vùng khác.

Cuối thập kỷ 1970 và đầu 1980, vài nhóm bắt đầu khám phá tác động của việc cắt bỏ một phần đầu vào cảm giác. Michael Merzenich, Jon Kaas và Doug Rasmusson phát hiện ra rằng -- và điều này đã được kiểm nghiệm ở rất nhiều lab -- nếu vùng vỏ não không nhận được tín hiệu đầu vào, sau một thời gian nó sẽ đáp ứng các tín hiệu khác, thường là ở bên cạnh. Nghiên cứu của Merzenich (1984) liên quan đến ánh xạ bàn tay của khỉ đêm trước và sau khi tháo bỏ ngón tay thứ ba. Ban đầu có năm vùng riêng biệt, mỗi vùng cho


study involved the mapping of owl monkey hands before and after amputation of the third digit. Before amputation, there were five distinct areas, one corresponding to each digit of the experimental hand. Sixty-two days following amputation of the third digit, the area in the cortical map formerly occupied by that digit had been invaded by the previously adjacent second and fourth digit zones. The areas representing digit one and five are not located directly beside the area representing digit three, so these regions remained, for the most part, unchanged following amputation.[10] This study demonstrates that only those regions that border a certain area invade it to alter the cortical map. In the somatic sensory system, in which this phenomenon has been most thoroughly investigated, JT Wall and J Xu have traced the mechanisms underlying this plasticity. 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.[11]

Merzenich and William Jenkins (1990) initiated studies relating sensory experience, without pathological perturbation, to cortically observed plasticity in the primate somatosensory system, with the finding that sensory sites activated in an attended operant behavior increase in their cortical representation. Shortly thereafter, Ford Ebner and colleagues (1994) made similar efforts in the rodent whisker barrel cortex (also somatic sensory system). These two groups largely diverged over the years. The rodent whisker barrel efforts became a focus for Ebner, Matthew Diamond, Michael Armstrong-James, Robert Sachdev, and Kevin Fox. Great inroads were made in identifying the locus of change as being at cortical synapses expressing NMDA receptors, and in implicating cholinergic inputs as necessary for normal expression. However, the rodent studies were poorly focused on the behavioral end, and Ron Frostig and Daniel Polley (1999, 2004) identified behavioral manipulations as causing a substantial impact on the cortical plasticity in that system.

Merzenich and DT Blake (2002, 2005, 2006) went on to use cortical implants to study the evolution of plasticity in both the somatosensory and auditory systems. Both systems show similar changes with respect to behavior. When a stimulus is cognitively associated with reinforcement, its cortical representation is strengthened and enlarged. In some cases, cortical representations can increase two to threefold in 1–2 days when a new sensory motor behavior is first acquired, and changes are largely finished within at most a few weeks. Control studies show that these changes are not caused by sensory experience alone: they require learning about the sensory experience, and are strongest for the stimuli that are associated with reward, and occur with equal ease in operant and classical conditioning behaviors.

An interesting phenomenon involving cortical maps is the incidence of phantom limbs. Phantom limbs are experienced by people who have undergone amputations in hands, arms, and legs, but it is not limited to extremities. Although the neurological basis of phantom limbs is still not entirely understood it is believed that cortical reorganization plays an important role.[12]

Norman Doidge, following the lead of Michael Merzenich, separates manifestations of neuroplasticity into adaptations that have positive or negative behavioral consequences. For example, if an organism can recover after a stroke to normal levels of performance, that adaptiveness could be considered an example of "positive plasticity". Changes such as an excessive level of neuronal growth leading to spasticity or tonic paralysis, or an excessive release of neurotransmitters in response to injury that could kill nerve cells, are "negative" plasticity. In addition, drug addiction and obsessive-compulsive disorder are deemed examples of "negative plasticity" by Dr. Doidge, as the synaptic rewiring resulting in these behaviors is also highly maladaptive.[12][13]

A 2005 study found that the effects of neuroplasticity occur even more rapidly than previously expected. Medical students' brains were imaged during the period when they were studying for their exams. In a matter of months, the students' gray matter increased significantly in the posterior and lateral parietal cortex.[14]

Applications and example

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 solid evidence that neurogenesis (birth of brain cells) occurs in the adult, mammalian brain—and such changes can persist well into old age.[2] The evidence for neurogenesis is mainly restricted to the hippocampus and olfactory bulb, but current research has revealed that other parts of the brain, including the cerebellum, may be involved as well.[15]

There is now ample evidence [cần dẫn nguồn] 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 epistemology referred to as 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.

Treatment of brain damage

A surprising consequence of neuroplasticity is that the brain activity associated with a given function can move 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 have evidence to 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.[16]

One group has developed a treatment that includes increased levels of progesterone injections to give to brain-injured patients. "Administration of progesterone after traumatic brain injury[17] (TBI) and stroke reduces edema, inflammation, and neuronal cell death, and enhances spatial reference memory and sensory motor recovery."[18] In their clinical trials, they had a group of severely injured patients that after the three days of progesterone injections had a 60% reduction in mortality.[19] A study published in the New 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.[20]

Vision

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 stereo vision anomalies have become prime examples of neuroplasticity; binocular vision improvements and stereopsis recovery are now active areas of scientific and clinical research.[21][22][23]

Treatment of learning difficulties

Michael Merzenich developed a series of "plasticity-based computer programs known as Fast ForWord.[24] FastForWord offers seven brain exercises to help with the language and learning deficits of dyslexia. In a recent study, experimental training was done in adults to see if it would help to counteract the negative plasticity that results from age-related cognitive decline (ARCD). The ET design included six exercises designed to reverse the dysfunctions caused by ARCD in cognition, memory, motor control, and so on. After use of the ET program for 8–10 weeks, there was a "significant increase in task-specific performance."[cần dẫn nguồn] The data collected from the study indicated that a neuroplasticity-based program could notably improve cognitive function and memory in adults with ARCD. However, a systematic meta-analytic review found that "There is no evidence from the analysis carried out that Fast ForWord is effective as a treatment for children's oral language or reading difficulties." [25]

Sensory prostheses

Neuroplasticity is involved in the development of sensory function. The brain is born immature and it adapts to sensory inputs after birth. In the auditory system, congenital hearing impairment, a rather frequent inborn condition affecting 1 of 1000 newborns, has been shown to affect auditory development, and implantation of a sensory prostheses activating the auditory system has prevented the deficits and induced functional maturation of the auditory system [26] 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 to learn mother language and acquire acoustic communication.[27]

Phantom limbs

A diagrammatic explanation of the mirror box. The patient places the good limb into one side of the box (in this case the right hand) and the amputated limb into the other side. Due to the mirror, the patient sees a reflection of the good hand where the missing limb would be (indicated in lower contrast). The patient thus receives artificial visual feedback that the "resurrected" limb is now moving when they move the good hand.
Bài chi tiết: Phantom limb và Mirror box

In the phenomenon of phantom limb, 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.[28] An explanation for this refers to 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 limbs 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.[29] Her research showed that phantom limb pain (rather than referred sensations) was the perceptual correlate of cortical reorganization.[30] This phenomenon is sometimes referred to as maladaptive plasticity.

In 2009 Lorimer Moseley and Peter Brugger carried out a remarkable experiment in which they encouraged arm amputee subjects to use visual imagery to contort their phantom limbs into impossible configurations. Four of the seven subjects succeeded in performing impossible movements of the phantom limb. This experiment suggests that the subjects had modified the neural representation of their phantom limbs and generated the motor commands needed to execute impossible movements in the absence of feedback from the body.[31] 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."

Chronic pain

Bài chi tiết: Chronic pain

Individuals who suffer from chronic pain experience prolonged pain at sites that may have been previously injured, yet are otherwise currently healthy. This phenomenon is related to neuroplasticity due to a maladaptive reorganization of the nervous system, both peripherally and centrally. During the period of tissue damage, noxious stimuli and inflammation cause an elevation of nociceptive input from the periphery to the central nervous system. Prolonged nociception from periphery then elicit a neuroplastic response at the cortical level to change its somatotopic organization for the painful site, inducing central sensitization.[32] 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.[33] 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.[34] 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,[35] chronic low back pain[36] and carpal tunnel syndrome.[37]

Meditation

Bài chi tiết: Research on meditation

A number of studies have linked meditation practice to differences in cortical thickness or density of gray matter.[38][39][40] One of the most well-known studies to demonstrate this was led by Sara Lazar, from Harvard University, in 2000.[41] Richard Davidson, a neuroscientist at the University of Wisconsin, has led experiments in cooperation with the Dalai Lama on effects of meditation on the brain. His results suggest that long-term, or short-term practice of meditation results in different levels of activity in brain regions associated with such qualities as attention, anxiety, depression, fear, anger, the ability of the body to heal itself, and so on. These functional changes may be caused by changes in the physical structure of the brain.[42][43][44][45]

Fitness and exercise

Xem thêm: Neurobiological effects of physical exercise § Structural growth

Aerobic exercise promotes adult neurogenesis by increasing 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).[46][47][48] Exercise-induced neurogenesis in the hippocampus is associated with measurable improvements in spatial memory.[49][50][51][52] 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.[48][49][53][54] The brain structures that show the greatest improvements in gray matter volume in response to aerobic exercise are the prefrontal cortex and hippocampus;[48][49][50] moderate improvements seen in the anterior cingulate cortex, parietal cortex, cerebellum, caudate nucleus, and nucleus accumbens.[48][49][50] Higher physical fitness scores (measured by VO2 max) are associated with better executive function, faster processing speed, and greater volume of the hippocampus, caudate nucleus, and nucleus accumbens.[49]

Human echolocation

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[55] and 2011[56] using functional 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.[57]

ADHD stimulants

Reviews of magnetic resonance imaging (MRI) studies on individuals with ADHD suggest that the long-term treatment of attention deficit hyperactivity disorder (ADHD) with stimulants, such as amphetamine or methylphenidate, decreases abnormalities in brain structure and function found in subjects with ADHD, and improves function in several parts of the brain, such as the right caudate nucleus of the basal ganglia.[58][59][60] Based upon rodent models, the authors of one review proposed that "juvenile exposure to methylphenidate may cause abnormal prefrontal function and impaired plasticity in the healthy brain".[61] The same authors noted in another review that in juvenile rats, methylphenidate reduced levels of NR2B subunit of the NMDA receptor without altering NR2A levels in the prefrontal cortex, thereby affecting long-term plasticity in the prefrontal cortex.[62]

In animals

Xem thêm: Brain development và Neural development in humans

In a single lifespan, individuals in 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.[63][64][65][66] Some changes occur seasonally in species to enhance or generate response behaviors.

Seasonal brain changes

Changing brain behavior and morphology to suit other seasonal behaviors is relatively common in animals.[67] These changes can improve the chances of mating during breeding season.[63][64][65][67][68][69] Examples of seasonal brain morphology change can be found within many classes and species.

Within the class Aves, black-capped chickadees experience an increase in the volume of the hippocampus and strength of neural connections to the hippocampus during fall months.[70][71] This change in brain morphology for spatial memory within the hippocampus is not limited to birds, and affects some rodents and amphibians.[67] In songbirds, many song control nuclei in the brain increase in size during mating season.[67] Among birds, changes in brain morphology to influence song patterns, frequency, and volume are common.[72] 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.[63][64]

The California sea hare, a gastropod, has more successful inhibition of egg-laying hormones outside of mating season due to increased effectiveness of inhibitors in the brain.[65] Changes to the inhibitory nature of regions of the brain can also be found in humans and other mammals.[66] In the amphibian Bufo japonicus, part of the amygdala is larger before breeding and during hibernation than it is after breeding.[68]

Seasonal brain variation occurs within many mammals. Part of the hypothalamus of the common ewe is more receptive to GnRH during breeding season than at other times of the year.[69] Humans experience a change in the "size of the hypothalamic suprachiasmatic nucleus and vasopressin-immunoreactive neurons within it"[66] during the fall, when these parts are larger. In the spring, both reduce in size.[73]

Operation of brain-machine interfaces

Brain-machine interface (BMI) is a rapidly developing field of neuroscience. According to the results obtained by Mikhail Lebedev, Miguel Nicolelis and their colleagues,[74] operation of BMIs results in incorporation of artificial actuators into brain representations. The scientists showed that modifications in neuronal representation of the monkey's hand and the actuator that was controlled by the monkey brain occurred in multiple cortical areas while the monkey operated a BMI. In these single day experiments, monkeys initially moved the actuator by pushing a joystick. After mapping out the motor neuron ensembles, control of the actuator was switched to the model of the ensembles so that the brain activity, and not the hand, directly controlled the actuator. The activity of individual neurons and neuronal populations became less representative of the animal's hand movements while representing the movements of the actuator. Presumably as a result of this adaptation, the animals could eventually stop moving their hands yet continue to operate the actuator. Thus, during BMI control, cortical ensembles plastically adapt, within tens of minutes, to represent behaviorally significant motor parameters, even if these are not associated with movements of the animal's own limb.

Active laboratory groups include those of John Donoghue at Brown, Richard Andersen at Caltech, Krishna Shenoy at Stanford, Nicholas Hatsopoulos of University of Chicago, Andy Schwartz at University of Pittsburgh, Sandro Mussa-Ivaldi at Northwestern and Miguel Nicolelis at Duke. Donoghue and Nicolelis' groups have independently shown that animals can control external interfaces in tasks requiring feedback, with models based on activity of cortical neurons, and that animals can adaptively change their minds to make the models work better. Donoghue's group took the implants from Richard Normann's lab at Utah (the "Utah" array), and improved it by changing the insulation from polyimide to parylene-c, and commercialized it through the company Cyberkinetics. These efforts are the leading candidate for the first human trials on a broad scale for motor cortical implants to help quadriplegic or locked-in patients communicate with the outside world.

Traumatic brain injury research

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.[75] With respect to the distal forelimb representation, "postinfarction mapping procedures revealed that movement representations underwent reorganization throughout the adjacent, undamaged cortex."[75] 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. Nudo is also involved in studying the treatment plans that may enhance recovery from strokes, such as physiotherapy, pharmacotherapy, and electrical-stimulation therapy.

Jon Kaas, a professor at Vanderbilt 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."[76] 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 when people damage the somatosensory cortex, impairment of the body perceptions are experienced. He is trying to see how these systems (somatosensory, cognitive, motor systems) are plastic as a result of injury.[76]

One of the most recent applications of neuroplasticity involves work done by a team of doctors and researchers at Emory University, specifically Dr. Donald Stein (who has been in the field for over three decades)[77] and Dr. David Wright. This is the first treatment in 40 years that has significant results in treating traumatic brain injuries while also incurring no known side effects and being cheap to administer.[19] Dr. Stein noticed that female mice seemed to recover from brain injuries better than male mice. Also in females, he noticed that at certain points in the estrus cycle females recovered even more. After lots of research, they attributed this difference due to the levels of progesterone. The highest level of progesterone present led to the fastest recovery of brain injury in these mice.

History

Origin

The term "plasticity" was first applied to behavior in 1890 by William James in The Principles of Psychology.[78] The first person to use the term neural plasticity appears to have been the Polish neuroscientist Jerzy Konorski.[1][79]

In 1793, Italian anatomist Michele Vicenzo Malacarne described experiments in which he paired animals, trained one of the pair extensively for years, and then dissected both. He discovered that the cerebellums of the trained animals were substantially larger. But, these findings were eventually forgotten.[80] The idea that the brain and its functions are not fixed throughout adulthood was proposed in 1890 by William James in The Principles of Psychology, though the idea was largely neglected.[78] Until around the 1970s, neuroscientists believed that brain's structure and function was essentially fixed throughout adulthood.[81]

The term has since seen 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.[82]

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 suggesting plasticity, neuroscientists did not widely accept the idea of neuroplasticity.

In 1945, Justo Gonzalo concluded from his research of brain dynamics, that, contrary to the activity of the projection areas, the "central" cortical mass (more or less equidistant from the visual, tactile and auditive projection areas), would be a "maneuvering mass", rather unspecific or multisensory, with capacity to increase neural excitability and re-organize the activity by means of plasticity properties.[83] He gives as a first example of adaptation, to see upright with reversing glasses in the Stratton experiment,[84] 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)].[83] 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.[85]

A 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.[81][86]

In the 1960s, Paul Bach-y-Rita invented a device that allowed blind people to read, perceive shadows, and distinguish between close and distant objects. This "machine was one of the first and boldest applications of neuroplasticity."[12] The patient sat in an electrically stimulated chair. Behind the chair, a large camera scanned the area, sending electrical signals of the image to four hundred vibrating stimulators on the chair against the patient’s skin. The six experimental subjects eventually could recognize a picture of the fashion model Twiggy.[12]

It must be emphasized that these people were congenitally blind. Bach-y-Rita believed in sensory substitution; if one sense is damaged, your other senses can sometimes take over. He thought the skin and its touch receptors could act as a retina (using one sense for another[87]). For the brain to interpret tactile information and convert it into visual information, it must learn something new and adapt to the new signals. The brain's capacity to adapt implied that it possessed plasticity. He thought, "We see with our brains, not with our eyes."[12]

A tragic stroke that left his father paralyzed inspired Bach-y-Rita to study brain rehabilitation. His brother, a physician, worked tirelessly to develop therapeutic measures that were so successful that the father recovered complete functionality by age 68, and was able to live a normal, active life that even included mountain climbing. "His father’s story was firsthand evidence that a ‘late recovery’ could occur even with a massive lesion in an elderly person."[12] He found more evidence of this possible brain reorganization with Shepherd Ivory Franz's work.[88] One study involved stroke patients who were able to recover through the use of brain stimulating exercises after having been paralyzed for years. "Franz understood the importance of interesting, motivating rehabilitation: ‘Under conditions of interest, such as that of competition, the resulting movement may be much more efficiently carried out than in the dull, routine training in the laboratory’(Franz, 1921, pg.93)."[89] This notion has led to motivational rehabilitation programs that are used today.

Eleanor Maguire documented changes in hippocampal structure associated with acquiring the knowledge of London’s layout in local taxi drivers.[90][91][92] 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 world-wide.

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."[12] 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."[12]

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."[12] Merzenich received the 2016 Kavli Prize in Neuroscience "for the discovery of mechanisms that allow experience and neural activity to remodel brain function."[93]

Notable studies

Hubel and Wiesel had demonstrated that ocular dominance columns in the lowest neocortical visual area, V1, remained largely immutable after the critical period in development.[94] Researchers also studied critical periods with respect to language; the resulting data suggested that sensory pathways were fixed after the critical period. However, studies determined that environmental changes could alter behavior and cognition by modifying connections between existing neurons and via neurogenesis in the hippocampus and in other parts of the brain, including in the cerebellum.[15]

Decades of research have shown that substantial changes occur in the lowest neocortical processing areas, and that these changes can profoundly alter the pattern of neuronal activation in response to experience. Neuroscientific research indicates that experience can actually change both the brain's physical structure (anatomy) and functional organization (physiology). Tính đến năm 2014, neuroscientists are engaged in a reconciliation of critical-period studies (demonstrating the immutability of the brain after development) with the more recent research showing how the brain can, and does, change in response to hitherto unsuspected stimuli.[95]

See also

References

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  47. ^ Szuhany KL, Bugatti M, Otto MW (tháng 10 năm 2014). “A meta-analytic review of the effects of exercise on brain-derived neurotrophic factor”. J Psychiatr Res. 60C: 56–64. doi:10.1016/j.jpsychires.2014.10.003. PMC 4314337. PMID 25455510. 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
  48. ^ a b c d Gomez-Pinilla F, Hillman C (tháng 1 năm 2013). “The influence of exercise on cognitive abilities”. Compr Physiol. 3 (1): 403–428. doi:10.1002/cphy.c110063. PMC 3951958. PMID 23720292. A second recent meta-analysis (162) corroborated Colcombe and Kramer’s (30) findings, in that aerobic exercise was related to attention, processing speed, memory, and cognitive control. ... Normal aging results in the loss of brain tissue (31), with markedly larger tissue loss evidenced in the frontal, temporal, and parietal cortices (16, 58, 149). As such, cognitive functions subserved by these brain regions (such as those involved in cognitive control and memory) are expected to decay more dramatically than other aspects of cognition. Specifically, age-related decreases in gray matter volume have been associated with decrements in a variety of cognitive control processes. ... Decreases in gray matter volume may result from several factors including loss in the number of neurons, neuronal shrinkage, reduction in dendritic arborization, and alterations in glia (158). Further, decreases in white matter (brain tissue composed primarily of myelinated nerve fibers) volume, which represent changes in connectivity between neurons, also occur as a result of aging. Loss of white matter volume further relates to performance decrements on a host of cognitive tasks ... aerobic fitness relates to larger hippocampal volume (23) and better relational memory performance (24), during preadolescent childhood. ... Specifically, those assigned to the aerobic training group demonstrated increases in gray matter in the frontal lobes, including the dorsal anterior cingulate cortex (ACC), supplementary motor area, middle frontal gyrus, dorsolateral region of the right inferior frontal gyrus, and the left superior temporal lobe (32). White matter volume changes were also evidenced for the aerobic fitness group with increases in white matter tracts within the anterior third of the corpus callosum (32). ... In addition, aerobic fitness has been shown to promote better functioning of brain, especially in neural networks involved in cognitive control of inhibition and attention (33). ... In addition to BDNF, the actions of IGF-1 and vascular endothelial growth factor (VEGF) (54) are considered essential for the angiogenic and neurogenic effects of exercise in the brain. ... Randomized and crossover clinical trials demonstrate the efficacy of aerobic or resistance training exercise (2–4 months) as a treatment for depression in both young and older individuals. ... exercise seems to have both preventative and therapeutic effects on the course of depression
  49. ^ a b c d e Erickson KI, Leckie RL, Weinstein AM (tháng 9 năm 2014). “Physical activity, fitness, and gray matter volume”. Neurobiol. Aging. 35 Suppl 2: S20–528. doi:10.1016/j.neurobiolaging.2014.03.034. PMC 4094356. PMID 24952993. Truy cập ngày 9 tháng 12 năm 2014. We conclude that higher cardiorespiratory fitness levels are routinely associated with greater gray matter volume in the prefrontal cortex and hippocampus and less consistently in other regions. We also conclude that physical activity is associated with greater gray matter volume in the same regions that are associated with cardiorespiratory fitness including the prefrontal cortex and hippocampus. ... Meta-analyses (Colcombe and Kramer, 2003; Smith et al., 2010) suggest that the effects of exercise on the brain might not be uniform across all regions and that some brain areas, specifically those areas supporting executive functions, might be more influenced by participation in exercise than areas not as critically involved in executive functions. ... The effects appear general in the sense that many different cognitive domains are improved after several months of aerobic exercise, but specific in the sense that executive functions are improved more than other cognitive domains. ... physical activity and exercise may reduce the risk for AD (Barnes and Yaffe, 2011; Podewils et al., 2005; Sofi et al., 2011) ... Erickson et al. (2010) reported that greater amounts of physical activity were associated with greater gray matter volume 9-years later in the prefrontal cortex, anterior cingulate, parietal cortex, cerebellum, and hippocampus. ... higher fitness levels (VO2max) were associated with larger hippocampal volumes, better executive function, and faster processing speed. ... Verstynen et al. (2012) examined the association between cardiorespiratory fitness levels (VO2max) and the size of the basal ganglia ... Verstynen et al. (2012) found that higher fitness levels were associated with greater volume of the caudate nucleus and nucleus accumbens, and in turn, greater volumes were associated with better performance on a task-switching paradigm. ... That is, higher physical activity levels mitigated the detrimental effects of lifetime stress on the size of the hippocampus. ... The few randomized interventions published thus far have found results highly overlapping with the cross-sectional studies and suggest that the prefrontal cortex and hippocampus remain pliable in late life and that moderate intensity exercise for 6 months–1 year is sufficient for changing the size of these areas.
  50. ^ a b c Erickson KI, Miller DL, Roecklein KA (2012). “The aging hippocampus: interactions between exercise, depression, and BDNF”. Neuroscientist. 18 (1): 82–97. doi:10.1177/1073858410397054. PMC 3575139. PMID 21531985. Late adulthood is associated with increased hippocampal atrophy and dysfunction.  ... However, there is strong evidence that decreased BDNF is associated with age-related hippocampal dysfunction, memory impairment, and increased risk for depression, whereas increasing BDNF by aerobic exercise appears to ameliorate hippocampal atrophy, improve memory function, and reduce depression. ... For example, longitudinal studies have reported between 1% and 2% annual hippocampal atrophy in adults older than 55 years without dementia ... Over a nine-year period, greater amounts of physical activity in the form of walking are associated with greater gray matter volume in several regions including prefrontal, temporal, and hippocampal areas. ... The prefrontal cortex and hippocampus deteriorate in late adulthood, preceding and leading to deficits in executive and memory function. We examined in this review the evidence that age-related changes in BDNF might at least partially explain hippocampal atrophy and increased risk for memory impairment. We can conclude that 1) decreases in BDNF protein expression are associated with poorer hippocampal function and increased rates of geriatric depression and AD. ... 3) Aerobic exercise enhances executive and memory function and reduces hippocampal atrophy in late adulthood, and this may be partially mediated through a BDNF pathway.
  51. ^ Lees C, Hopkins J (2013). “Effect of aerobic exercise on cognition, academic achievement, and psychosocial function in children: a systematic review of randomized control trials”. Prev Chronic Dis. 10: E174. doi:10.5888/pcd10.130010. PMC 3809922. PMID 24157077. This omission is relevant, given the evidence that aerobic-based physical activity generates structural changes in the brain, such as neurogenesis, angiogenesis, increased hippocampal volume, and connectivity (12,13). In children, a positive relationship between aerobic fitness, hippocampal volume, and memory has been found (12,13). ... Mental health outcomes included reduced depression and increased self-esteem, although no change was found in anxiety levels (18). ... This systematic review of the literature found that APA is positively associated with cognition, academic achievement, behavior, and psychosocial functioning outcomes. Importantly, Shephard also showed that curriculum time reassigned to APA still results in a measurable, albeit small, improvement in academic performance (24).  ... The actual aerobic-based activity does not appear a major factor; interventions used many different types of APA and found similar associations. In positive association studies, intensity of the aerobic activity was moderate to vigorous. The amount of time spent in APA varied significantly between studies; however, even as little as 45 minutes per week appeared to have a benefit.
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Further reading

Videos
Other readings
  • Chorost, Michael (2005). Rebuilt: how becoming part computer made me more human. Boston: Houghton Mifflin. ISBN 0-618-37829-4.

External links

Bản mẫu:Neuroscience Bản mẫu:Nervous system physiology

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