Psychology
Neural Plasticity
Neural plasticity refers to the brain's ability to reorganize itself by forming new neural connections throughout life. It allows the brain to adapt to experiences, learn new information, and recover from injuries. This process is essential for learning and memory, and it underlies the brain's ability to recover from damage and adapt to changes in the environment.
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11 Key excerpts on "Neural Plasticity"
eBook - PDFTraumatic Brain and Spinal Cord Injury
Challenges and Developments
- Cristina Morganti-Kossmann, Ramesh Raghupathi, Andrew Maas(Authors)
- 2012(Publication Date)
- Cambridge University Press(Publisher)
Section 1 Traumatic Brain Injury Chapter 15 Plasticity and recovery of the injured brain Dorothy A. Kozlowski and Theresa A. Jones Introduction Neuroplasticity is the ability of the nervous system to change itself, as it does in response to experiences and to injury. Neuroplasticity is not a novel idea. In 1890, the psychologist, William James, proposed it to be the mechanism underlying the formation of motor, intellectual and professional skills, and other “habits” [1]. Neuroanatomical plasticity was also described in exquisite detail by Ram´ on y Cajal in the late nine- teenth and early twentieth centuries in his studies of the diseased brain [2]. The idea that learning occurs as a result of activity-dependent modifications in neural circuitry gained prominence in 1949, with Donald Hebb’s profoundly influential postulate that (as com- monly simplified) neurons that fire together, wire together [3]. Nevertheless, Neural Plasticity continued to be viewed as largely a developmental phenomenon. In the 1960s, Hubel and Wiesel strengthened this belief and instituted the idea that there was a “critical period” for neuroplasticity. They found that depriving one eye of visual stimulation during a specific develop- mental time window in young kittens, but not in adult cats, produced blindness and significantly affected the development of the visual cortex by eliminating ocular dominance columns [4]. This idea of neuroplasticity as a developmental phenomenon persisted into the 1970s. It was around this time that Greenough and others found that mature cortical neurons in rats can grow new dendrites and synapses in response to behav- ioral manipulations, such as housing in an enriched environment or maze training. This was found first in rats that were juvenile, but past early critical periods of development [5], and soon after it was found in fully adult rats [6, 7].
eBook - PDFThe Brain's Body
Neuroscience and Corporeal Politics
- Victoria Pitts-Taylor(Author)
- 2016(Publication Date)
- Duke University Press Books(Publisher)
At the start of modern neuro-science, the concept of plasticity emerged to address how neurons’ connec-tions with each other are related to the brain’s activity. In the mid-twentieth century, this synaptic or “functional” plasticity often was elaborated in con-trast to the apparently fixed structural organization of the brain. Evidence of the mature brain’s ability to rewire and reshape itself in response to new stimuli and activity has more recently led to biosocial models of brain structure as well as function. This history should not be conceived in a tel-eological fashion, where the brain is merely awarded greater plasticity over time. Even in the current moment, when Neural Plasticity is more broadly recognized than ever before, the brain does not appear to be globally or monolithically plastic. Rather, in different research programs plasticity is unevenly distributed across developmental time scales, various regions of the brain, and even potentially between persons. 24 CHAPTER ONE Habit, Learning, and Synaptic Plasticity The term plasticity was used in eighteenth-century materials science to describe the malleability of matter, and in the nineteenth century to denote the ability of organisms to change in response to environmental demands (Berlucchi and Buchtel 2009). Early scientific conceptions of neural plas-ticity seem to have some relation to both meanings of the term. William James (1890), for example, noted that all matter, including nervous tissue, changes structure in the face of a “modifying cause.” He defined plasticity as the possession of a structure weak enough to yield to an influence, but strong enough not to yield at once. Matter changes, and it resists change; James argued that the dual ability of neurobiological matter to both modify and stabilize, in relation to the behaviors of persons, explains why people develop habits or characteristic propensities.
eBook - PDFNeuroplasticity
Insights of Neural Reorganization
- Victor V. Chaban(Author)
- 2018(Publication Date)
- IntechOpen(Publisher)
This brings us to the concept of brain plasticity, which refers to the fact that neuronal circuits are tuned in close interaction with the environment. It was introduced by William James, who defined plasticity as “the possession of a structure weak enough to yield to an influence, but strong enough not to yield all at once” [ 44] (p. 106). The idea was further devel-oped by Ramón y Cajal, who claimed that to fully understand the phenomenon it is necessary to admit the formation of new pathways in the brain through ramification and progressive growth of the dendritic arborisation and the nervous terminals in addition to the reinforce-ment of pre-established organic pathways. The same idea was elaborated further by Donald Hebb, who proposed that neuronal cortical connections are strengthened and remodelled by experience. There is, however, another aspect of plasticity that goes beyond the level of Neuroplasticity - Insights of Neural Reorganization 88 synapses and that incorporates the level of cortical representation areas or cortical maps, which can be modified by sensory input and training [ 45]. It is suggested, in this regard, that additional neurons are recruited when they are needed and that rapid and transient altera-tions of cortical representations can be seen during learning tasks. Such short-term modu-lations are important in the acquisition of new skills, but they can lead also to structural changes in the intra-cortical and sub-cortical network once the skill has been established. 3. Neuroplasticity and music: macrostructural and microstructural adaptations The evolutionary claims of adaptation—both at the phylogenetic and ontogenetic level—have received empirical evidence from neuroimaging and morphometric studies. In order to elu-cidate its underlying mechanisms, there is currently a whole body of research related to the psychobiological approach to the study of action, cognition and perception.
eBook - PDFImproving Hand Function in Children with Cerebral Palsy
Theory, Evidence and Intervention
- Ann-Christian Eliasson, Patricia Burtner(Authors)
- 2008(Publication Date)
- Mac Keith Press(Publisher)
1 BRAIN PLASTICITY IN DEVELOPMENT AND DISEASE Hans Forssberg Introduction The term brain plasticity was introduced around 100 years ago. It is used to describe how the structure and function of neural circuits are modified (1) during development, (2) by experience and learning, and (3) in response to brain lesions. In the middle of the last century, Donald Hebb postulated that cortical neural connections, i.e. synapses, are strengthened and remodelled by experience (Hebb et al 1994). He also showed that rats reared in the rich environment of his own house were much better learners and had better memory capacity than rats living in laboratory cages. The molecular mechanisms behind Neural Plasticity are complex and not yet fully understood, but numerous studies have shown various mechanisms underlying the activity-dependent modification of synaptic connectivity, including increased number of synapses by changed turnover of dendritic spines, long-term potentiation (LTP) and long-term depression (LDP) (Calverley and Jones 1990, Jenkins et al 1990, Buonomano and Merzenich 1998, Feldman et al 1999, Luscher et al 2000, Trachtenberg et al 2002, Malenka 2003). The latter two mechanisms are important for storage of information in the central nervous system (CNS) and involve several neurotransmitter systems, including gluta-mate (NMDA and AMPA receptors) and GABA (Myers et al 2000), as well as the monoamine systems (dopamine, noradrenalin and serotonin), which are involved by modulating the transmission in the other neurotransmitter systems (Bao et al 2001, Gu 2002). Neuroimaging methods used to study brain plasticity The first studies on Neural Plasticity were performed in experiments on animals. More recently, the development of new powerful imaging techniques has made it possible to study Neural Plasticity in the human brain as well. Magnetic resonance imaging (MRI) is the most widely used method and enables studies on both structure and function.
eBook - PDFSynaptic Plasticity
Basic Mechanisms to Clinical Applications
- Michel Baudry, Xiaoning Bi, Steven S. Schreiber(Authors)
- 2005(Publication Date)
- CRC Press(Publisher)
By plasticity in this context, we refer to adap-tive events affecting the morphology, anatomical connections, and the func-tions subserved by neurones. Particular attention is paid to the relationship between host and transplanted cells, the anatomical integration of the grafted cells, and how circuit reconstruction within the host brain might promote functional recovery. Furthermore, we examine the role of the environment and the experience of the individual suffering from brain damage or disease. Together, these data indicate that rehabilitative train-ing has the potential to modify the functional plasticity both of the affected brain and of the transplants. The different mechanisms by which cells from different sources, and following different types of brain damage, can affect host function will also determine their dependence on training and experience for maximizing therapeutic outcome. During the period immediately following injury and during the early stages of disease, the brain is at its most plastic and privileged state, offering a window of opportunity for therapeutic intervention. In contrast to a pes-simistic interpretation of Cajal’s dictum, cited above, spontaneous recovery following injury shows that the adult brain does retain the capacity at some level to reorganize itself functionally. In order to improve the outcome fol-lowing brain damage, cell replacement therapy must both make use of the endogenous potential for recovery of the host and optimize the external circumstances associated with any intervention, such as the source and treatment of the cells, the timing of the intervention, and the experience and the environment of the recipient. The role of these factors in neural plas-ticity and transplant-induced brain repair is examined in more detail in the following sections.
- M.A. Hofman, G.J. Boer, Eus JW Van Someren, J. Verhaagen, D.F. Swaab, A.J.G.D. Holtmaat(Authors)
- 2002(Publication Date)
- Elsevier Science(Publisher)
Following a description of the multiple types of brain plasticity, experimental methods for dissociating the specific components of experience will be discussed. Neuronal and synaptic plasticity Among the most exciting recent developments in the field of Neural Plasticity are the data suggesting that the brain responds to experience by adding new neurons (neurogenesis). Using a thymidine analog (BrdU) that incorporates into replicating DNA, it has been demonstrated that neurogenesis occurs in the hippocampal formation following housing in a complex environment (Kempermann et al., 1998a,b; Nilsson et al., 1999). More specifically, using a learning paradigm in which the underlying neural pathways necessary to perform the task have been very well-characterized, it was reported that the rate of neurogenesis is dramatically increased in the hip-pocampus when this structure is critically involved in learning the task, yet when the contingency does not 93 demand involvement of this structure, neurogenesis is unaffected (Gould et al., 1999). Although these increases in neuron number are small relative to the number of neurons already present in the brain, the-ories of brain plasticity that have largely focused on changes in the number and strength of synapses in neural networks must now consider the profound effects that integration of new neurons could have on both the composition and function of these networks. While neurogenesis represents an exciting area, it is a principal focus of other chapters in this volume. Thus, we highlight here specific aspects of plasticity of existing neurons as they relate to elements of non-neuronal plasticity and to the functional implications of the existence of multiple forms of brain plasticity. Plasticity of synapse number At an anatomical level, the malleability of neuronal systems and individual neurons can be quantified using a number of parameters.
eBook - PDF- Thomas Heinbockel(Author)
- 2017(Publication Date)
- IntechOpen(Publisher)
The presented set of reviewed literature on plasticity in multisensory networks may have important implications regarding teaching, learning and rehabilitation strategies in persons with damage to the above described Synaptic Plasticity 124 brain areas. These findings indicate that the brain is capable of plastic changes throughout the lifespan, and even in healthy individuals, the brain seems to be always changing as a function of training and expertise. However, it is essential to make note that plasticity changes are intrinsic properties of the central nervous system, and thus, neural plastic changes do not always lead to a behavioral gain, but instead could be deleterious. Thus, more research should be focused on modulation of Neural Plasticity for optimal behavioral gain across all different types of individuals. Author details Karolina A Bearss 1 and Joseph FX DeSouza 1,2* *Address all correspondence to: [email protected] 1 Department of Psychology, Centre for Vision Research, York University, Toronto, ON, Canada 2 Biology and Interdisciplinary Studies, York University, Toronto, ON, Canada References [1] Graziano MS. A system of multimodal areas in the primate brain. Neuron. 2001;29:4–6. [2] Jones EG, Powell TP. An anatomical study of converging sensory pathways within the cerebral cortex of the monkey. Brain. 1970;93:793–820. [3] Chavis DA, Pandya DN. Further observations on corticofrontal connections in the rhe-sus monkey. Brain Research. 1976;117:369–386. [4] Seltzer B, Pandya DN. Converging visual and somatic sensory cortical input to the intra -parietal sulcus of the rhesus monkey. Brain Research. 1980;192:339–351. [5] Mufson EJ, Mesulam MM. Thalamic connections of the insula in the rhesus monkey and comments on the paralimbic connectivity of the medial pulvinar nucleus. Journal of Comparative Neurology. 1984;227:109–120. [6] Fries W. Cortical projections to the superior colliculus in the macaque monkey: a ret-rograde study using horseradish peroxidase.
eBook - PDFApplied Developmental Science
An Advanced Textbook
- Richard M. Lerner, Francine Jacobs, Donald Wertlieb, Richard M. Lerner, Francine Jacobs, Donald Wertlieb(Authors)
- 2005(Publication Date)
- SAGE Publications, Inc(Publisher)
Inherent in both experience-expectant and experience-dependent models is the notion that “experience cuts both ways.” By this, it is meant that the nature of the experience itself—coupled with the maturity of the brain at the time the experience occurs—will deter-mine (or at least influence) whether the result-ing neural change is beneficial or deleterious to the organism. In the sections that follow, I provide examples of both good and bad out-comes, as well as examples of plasticity that are restricted to the developing organism and those that are seemingly unconstrained by age. I shall begin, however, by discussing some general principles that account for how the structure of experience is incorporated into the structure of the brain. NEUROBIOLOGICAL MECHANISMS UNDERLYING Neural Plasticity As a rule, there are a number of mechanisms whereby experience induces changes in the brain. An anatomical change might reflect the ability of an existing synapse to modify its activity by forming new axons or by expanding the dendritic surface. For exam-ple, as we shall see in the section on learning and memory, rearing rats in complex environments can lead to an increase in den-dritic spines, which will ultimately lead to the formation of new synapses. A neurochemical change might be reflected in the ability of an existing synapse to modify its activity by increasing neurotransmitter synthesis and release. For example, is it now well estab-lished that NMDA, an excitotoxic amino acid used to identify a specific subset of glu-tamate, is known to modify pre- and postsy-naptic activity and can trigger the formation of new dendritic spines (for review, see Yuste & Sur, 1999). Third, an example of a metabolic change might be the fluctuations in cortical and subcortical metabolic activity (e.g., glucose usage, O 2 ) in response to expe-rience.
- Aage R. Møller(Author)
- 2010(Publication Date)
- Cambridge University Press(Publisher)
(Some inves- tigators have called this form of Neural Plasticity “environmental regulation of nervous system development” [100], whereas other investigators have used the term Neural Plasticity.) The mature nervous system was earlier regarded as being relatively stable, except for changes that are related to aging. The demonstration of the “kindling phenomenon” (in rats) by Goddard [34] was one of the first published reports that indicates that the function of the adult nervous system can be changed by external factors (electrical stimulation of the amygdala). Later, many studies have brought evidence that the function of the mature nervous system can be changed within wide limits through expression of Neural Plasticity [42, 46, 54, 72, 96, 99, 105, 111, 112, 119, 121]. While the expression of Neural Plasticity that is prominent in childhood can proceed throughout the entire life, the ability of the nervous system to change 12 Anatomical and physiological basis for Neural Plasticity its function after the critical postnatal period decreases with age. For exam- ple, while individuals who lose vestibular function at a young age can recover totally relatively quickly, older individuals take longer time to recover and the recovery is not complete. This is an example of adaptation to changing demands that occurs through changes in function and re-routing of neural information. Such switching of functions takes a considerably longer time with increasing age and it becomes incomplete if the injury occurs after a certain age of the individual, again indicating that the young organism is more flexible than the mature organism. Above the age of 60 years, recovery from loss of vestibular function is incomplete (see Chapter 6). This means expression of neural plastic- ity that is necessary for switching the functions that are normally provided by the vestibular system (such as control of posture) to other systems (such as pro- prioceptive systems) decreases with age.
eBook - PDF- Jon C. Horvitz, Barry L. Jacobs(Authors)
- 2022(Publication Date)
- Cambridge University Press(Publisher)
The irony of this situation should not be lost on us because these same events involving glutamate, its receptors, and Ca2 + are critical processes in virtually all positive forms of plasticity, including learning and memory. So, here we have the classi- cal case of too much of a good thing! KEY CONCEPTS • Neurotrophic factors are released by target neurons to promote the growth and survival of incoming axons. • Long-term potentiation is the strengthening of synaptic connections between neurons. Changes in synaptic strength play an important role in learning and memory. • In addition to trauma to the brain, the environment contains agents that are potentially harmful to the cells of the nervous system. • Excessive neuronal excitation is the primary mechanism underlying cell death. 8.2 PLASTICITY 337 8.2.5 Biological Processes and Technologies Offer Hope for CNS Recovery There is an intense interest in developing treatments that will promote re- covery after injury to the nervous system from disease or accidents. When we ask about nervous system recovery, there are several questions of in- terest. Can the damaged neurons reestablish their connections with their targets? If not, can other neurons that are not damaged take over some of their functions? Even if the damaged neurons fail to reestablish normal connections and healthy neurons do not substitute for them, the person may learn strategies to compensate for the movement difficulties or other disrupt- ed functions. For instance, if brain damage causes paralysis of one arm, the person may gain skill in using the unaffected arm to carry out more tasks. If elbow movements are no longer possible, the person may learn to carry out tasks by moving other joints in ways that compensate for the lost abilities. We begin with a brief discussion of the peripheral nervous system, where damaged neurons can often spontaneously reestablish their con- nections.
- Floyd E. Bloom(Author)
- 1994(Publication Date)
- Elsevier Science(Publisher)
This means that environment and training can model and alter neuronal properties in an adaptive manner. The functional reorganization seen in Jenkins’ work occurs far more rapidly than could be explained by the physical regeneration of nerve pathways themselves. The findings suggest that there are ‘‘latent” or “silent” pathways that occur in the normal development of the CNS. Such pathways can be unmasked and modified by experience or injury and later play a role in the re- covery process. Although there are many questions that could be addressed in more detail, two with par- ticular clinical relevance will close my review. The first is concerned with how soon after injury, the treatment should begin. Thanks to a large body of re- cent laboratory research, it is now quite clear that early and aggressive intervention and therapy may lead to the best prognosis for recovery. It has to be emphasized, here again, that brain injury and the con- comitant neuronal loss is not a single, unitary event. Rather, a cascade of processes, some of which may last for years, is the complex result of neural damage. For example, in the first stage(s) of injury, substances in the brain itself are produced which are toxic to neu- rons and which diffuse beyond the immediate area of the injury to kill or damage vulnerable cells (Nieto- Sampedro, 1988; McIntosh, 1993). Toxic substances can also enter through the blood supply or through a compromised blood-brain barrier, leading to inflam- mation and immune reactions. As a result, neurons 209 initially spared by the trauma could begin to die in massive numbers resulting in cell loss more devastat- ing to the patient than the initial injury itself. This is one reason why research on how much time should be devoted to rehabilitation or other forms of post-injury “therapy” is another area that needs careful investigation.
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