Brain Plasticity Year 11 2019

Total Page:16

File Type:pdf, Size:1020Kb

Brain Plasticity Year 11 2019 THE PLASTICITY OF THE BRAIN Neuroplasticity: The ability of the brain to form and reorganise synaptic connections, especially through learning or experience or following injury. This means that the brain… • is adaptive. • changes as a result of experience and learning. • creates new connections between neurons as we learn and experience the world. https://en.oxforddictionaries.com/definition/neuroplasticity A living example of the brain’s plasticity... The story of Jodie, whose right hemisphere had to be removed as a result of epileptic seizures. LINK TO THIS VIDEO Plasticity - More Details ✤ The brain can reorganise and reassign its neural connections and pathways based on which parts of it are used often or used rarely. ✤ Some areas of the brain, such as the sensory and motor cortices, have a higher level of plasticity than others. Especially plastic… Plasticity - Children ✤ A young child’s brain is more plastic than that of an adult, particularly at specific times in development. Strengthened Neural Connections ✤ Whenever you form new memories, the neural connections underlying them are strengthened. Each time these After repeated stimulation,... connections are activated, the neurons involved communicate more efficiently. …a stronger neural connection develops. Long-Term Potentiation ✤ Definition: The lasting strengthening of the synaptic connections of neurons, resulting in their enhanced functioning Long-Term Potentiation ✤ The more a particular neural pathway is activated, the easier it is for information to travel through that circuit. …rather like a bush path that becomes easier to walk along after many other hikers have cleared the way… Winner of the Nobel Prize for Medicine/Physiology in 2000 Eric Kandel If you remember anything about a book (or lecture), it will be because your brain is slightly different after you have finished reading (or hearing) it. When you learn something, your brain changes. That’s plasticity. Effects of Mental Stimulation and Deprivation 1 •Autopsies have shown that the brains of university graduates have 40% more synaptic connections than those of students who do not finish high school (Hockenbury and Hockenbury, 2006). Effects of Mental Stimulation and Deprivation 2 •The risk of cognitive decline in old age has been found to be reduced by doing mentally stimulating tasks, including social interaction and extensive reading. Effects of Mental Stimulation and Deprivation 3 •Studies with sets of identical twins have shown that the twin who was not mentally active or who had a lower level of education was more likely to develop Alzheimer’s Disease. The Story So Far 1: An Either-Or Quiz a The brain is ______ according to learning and experience. able to adapt unable to adapt b Which age group has greater brain plasticity? adults children c Which parts of the brain show the greatest ability to respond to experience? sensory and motor cortices cerebellum d The more often a particular neural pathway is activated the less efficient it becomes. the more efficient it becomes. e The lasting strengthening of synaptic connections, which allows enhanced communication between neurons, is called… consolidation long-term potentiation Two Kinds of Plasticity Developmental Plasticity Adaptive Plasticity occurs as brain is evident when the brain development proceeds recovers from trauma due to according to its normal brain injury and also when maturational blueprint or changes in brain structure plan. enable adjustment to experience. Developmental plasticity refers to changes in the brain’s neural structure in response to experience during the brain’s growth and development. Adaptive plasticity refers to the brain’s ability following brain injury to compensate for the damage done by developing new neural connections. Distinctions Note: A clear line cannot easily be drawn between the two types of plasticity. •Both types of plasticity are influenced by experience. •As Jodie’s recovery after her radical surgery illustrates, the maturing brain of a child has the capacity to adapt to and therefore recover from trauma effectively. Synaptogenesis Synapses are brain structures that permit neurons to send an electrochemical signal to another neuron. The creation of such connections is called synaptogenesis. Each neuron in a baby’s brain at birth already synapses with about 2500 other neurons. By the age of 2 or 3, the number of these connections will have increased dramatically, to around 15,000 per neuron. Link: University of Maine Website - Children’s Development Synaptic Pruning By about 10 years of age, almost 50% of the synapses that were present at the age of 2 will have been pruned or eliminated. This increases the efficiency of neural transmission and brain communication. This process is called synaptic pruning. Source: Santos E., Noggle C.A. (2011) Synaptic Pruning. In: Goldstein S., Naglieri J.A. (eds) Encyclopedia of Child Behavior and Development. Springer, Boston, MA The Story So Far 2: An Either-Or Quiz a The creation of new neural connections is called… synaptic pruning synaptogenesis b The elimination of unused neural connections is called… synaptic pruning synaptogenesis c Which type of plasticity refers to the brain’s ability to recover after trauma or injury? adaptive plasticity developmental plasticity d Synaptic pruning is essential because it makes neural transmission… less efficient. more efficient. e When does synaptogenesis occur most rapidly? 0-2 years of age 10-12 years of age f Which factor determines which synapses are retained? age of synapses use of synapses A Sensitive Period A sensitive (or critical) period is a specific period of time in development when an organism is more ‘sensitive’ or responsive to certain environmental stimuli or experiences. For example, another language is most easily acquired during a sensitive period in development and is more difficult and time-consuming to learn outside this ‘window of opportunity’. A Sensitive Period In relation to language learning, psychologists are not in complete agreement about the age limits for the sensitive period. Generally, the sensitive period for our native language is up to the age of about 12 years, with the window gradually closing from about age seven. The Importance of the Sensitive (or Critical) Period 1 Genie Genie, a girl who was deprived of language in the first 12 years of life through living in a kind of enforced solitary confinement, learned to speak yet was not able to develop all the standard language structures. It is however very difficult to determine which factors influenced this outcome. The Importance of the Sensitive (or Critical) Period 2 This child developed a haemangioma on her right eye as a young baby. The Importance of the Sensitive (or Critical) Period 2 Doctors warned that if this growth obscured her vision in the first year or two of life, there might never be sight in that eye. The eye itself would have been intact but the time when the brain makes connections with that eye’s input would have passed. The Importance of the Sensitive (or Critical) Period 2 Lack of stimulation during this sensitive period can lead to a long-term deficit. For instance, a closed eye from birth leads to later blindness in that eye, even when the eye eventually opens. A Happy Ending This child was lucky. Her haemangioma never did obscure her vision and she is now a fully sighted child. Adaptive Plasticity: Neuronal Changes Re-routing: Damaged parts of the brain begin to “rewire”, creating new neural pathways to replace older, damaged ones. Sprouting: The growth of new bushier nerve fibres with more branches on axons and dendrites. This facilitates new neural connections. When an accident occurs on a major road, travellers have to detour… Example: from this blog on MS research: https://drkarenlee.ca/rewiring-neurons-how-the-brain-copes-with-ms/ Another Form of Adaptive Plasticity When we learn a skill, this learning is becomes evident in the brain’s structure. In one study, the grey matter in the mid- temporal lobes of people who developed juggling skills increased by 3-4%. See also: http://faculty.washington.edu/chudler/jugg.html Adaptive Plasticity and Experience 1 Neuroimaging studies show that in musicians who play string instruments, the area of the somatosensory cortex that represents the fingers of the left hand is larger than the area that represents the fingers on the right hand. Adaptive Plasticity and Experience 2 MRI scans of London taxi drivers show that the rear of their hippocampus, the part involved in spatial navigation and consolidation of memories, is clearly larger than those of bus drivers, whose navigation skills are far less challenging. The Story So Far 3: Matching Concepts a long-term potentiation • b motor and sensory cortices • c plasticity • d rerouting • e synaptic pruning • f synaptogenesis 1 The lasting strengthening of synaptic connections of neurons, resulting in their enhanced functioning 2 The process of forming new synapses 3 An undamaged neuron, having lost a connection with a neuron, connects with another 4 The particularly plastic parts of the brain that are responsible for processing of movement and touch 5 The brain’s ability to rewire and adapt its neurons and its neural network as a result of learning and experience 6 The elimination of unused neural connections, particularly evident between ages 2 and 10.
Recommended publications
  • Developmental Plasticity of the Glutamate Synapse: Roles of Low Frequency Stimulation, Hebbian Induction and the Nmda Receptor
    DEVELOPMENTAL PLASTICITY OF THE GLUTAMATE SYNAPSE: ROLES OF LOW FREQUENCY STIMULATION, HEBBIAN INDUCTION AND THE NMDA RECEPTOR Akademisk avhandling som för avläggande av medicine doktorsexamen vid Sahlgrenska akademin vid Göteborgs universitet kommer att offentligen försvaras i hörsal 2119, Hus 2, Hälsovetarbacken Göteborg, fredagen den 12 februari 2010 kl 09.00 av Joakim Strandberg Fakultetsopponent: Professor Martin Garwicz Institutionen för experimentell medicinsk vetenskap Lunds universitet Avhandlingen baseras på följande delarbeten: I. Strandberg J., Wasling P. and Gustafsson B. Modulation of low frequency induced synaptic depression in the developing CA3-CA1 hippocampal synapses by NMDA and metabotropic glutamate receptor activation. Journal of Neurophysiology (2009) 101:2252-2262 II. Strandberg J. and Gustafsson B. Lasting activity-induced depression of previously non-stimulated CA3-CA1 synapses in the developing hippocampus; critical and complex role of NMDA receptors. In manuscript III. Strandberg J. and Gustafsson B. Hebbian activity does not stabilize synaptic transmission at CA3-CA1 synapses in the developing hippocampus. In manuscript Göteborg 2010 DEVELOPMENTAL PLASTICITY OF THE GLUTAMATE SYNAPSE: ROLES OF LOW FREQUENCY STIMULATION, HEBBIAN INDUCTION AND THE NMDA RECEPTOR Joakim Strandberg Department of Physiology, Institute of Neuroscience and Physiology, Univeristy of Gothenburg, Sweden, 2010 Abstract The glutamate synapse is by far the most common synapse in the brain and acts via postsynaptic AMPA, NMDA and mGlu receptors. During brain development there is a continuous production of these synapses where those partaking in activity resulting in neuronal activity are subsequently selected to establish an appropriate functional pattern of synaptic connectivity while those that do not are elimimated. Activity dependent synaptic plasticities, such as Hebbian induced long-term potentiation (LTP) and low frequency (1 Hz) induced long-term depression (LTD) have been considered to be of critical importance for this selection.
    [Show full text]
  • Specific Involvement of Postsynaptic Glun2b- Containing NMDA
    Specific involvement of postsynaptic GluN2B- containing NMDA receptors in the developmental elimination of corticospinal synapses Takae Ohnoa, Hitoshi Maedaa, Naoyuki Murabea, Tsutomu Kamiyamaa, Noboru Yoshiokaa, Masayoshi Mishinab, and Masaki Sakuraia,1 aDepartment of Physiology, School of Medicine, Teikyo University, Tokyo 173-8605, Japan; and bDepartment of Molecular Neurobiology and Pharmacology, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan Edited* by Masao Ito, RIKEN Brain Science Institute, Wako, Japan, and approved July 19, 2010 (received for review July 15, 2009) The GluN2B (GluRε2/NR2B) and GluN2A (GluRε1/NR2A) NMDA re- spinal gray matter at 7 d in vitro (DIV) but the synapses on the ceptor (NMDAR) subtypes have been differentially implicated in ventral side were subsequently eliminated through a process that activity-dependent synaptic plasticity. However, little is known was blocked by an NMDAR antagonist (22, 23). This type of about the respective contributions made by these two subtypes synapse elimination was also seen in vivo in the rat and followed to developmental plasticity, in part because studies of GluN2B KO a time course similar to that seen in vitro (24), and similar − − − − [Grin2b / (2b / )] mice are hampered by early neonatal mortality. elimination of synapses from ventral areas of the SpC during We previously used in vitro slice cocultures of rodent cerebral development has also been observed in cats (reviewed in ref. 25). cortex (Cx) and spinal cord (SpC) to show that corticospinal (CS) Those findings, together with the observation that the major synapses, once present throughout the SpC, are eliminated from NMDAR subunit mediating CS excitatory postsynaptic currents the ventral side during development in an NMDAR-dependent (EPSCs) appears to shift from 2B to 2A early during development manner.
    [Show full text]
  • Synaptogenesis and Development of Pyramidal Neuron Dendritic Morphology in the Chimpanzee Neocortex Resembles Humans
    Synaptogenesis and development of pyramidal neuron dendritic morphology in the chimpanzee neocortex resembles humans Serena Bianchia,1,2, Cheryl D. Stimpsona,1, Tetyana Dukaa, Michael D. Larsenb, William G. M. Janssenc, Zachary Collinsa, Amy L. Bauernfeinda, Steven J. Schapirod, Wallace B. Bazed, Mark J. McArthurd, William D. Hopkinse,f, Derek E. Wildmang, Leonard Lipovichg, Christopher W. Kuzawah, Bob Jacobsi, Patrick R. Hofc,j, and Chet C. Sherwooda,2 aDepartment of Anthropology, The George Washington University, Washington, DC 20052; bDepartment of Statistics and Biostatistics Center, The George Washington University, Rockville, MD 20852; cFishberg Department of Neuroscience and Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY 10029; dDepartment of Veterinary Sciences, The University of Texas MD Anderson Cancer Center, Bastrop, TX 78602; eNeuroscience Institute and Language Research Center, Georgia State University, Atlanta, GA 30302; fDivision of Developmental and Cognitive Neuroscience, Yerkes National Primate Research Center, Atlanta, GA 30322; gCenter for Molecular Medicine and Genetics, Wayne State University, Detroit, MI 48201; hDepartment of Anthropology, Northwestern University, Evanston, IL 60208; iDepartment of Psychology, Colorado College, Colorado Springs, CO 80903; and jNew York Consortium in Evolutionary Primatology, New York, NY 10024 Edited by Francisco J. Ayala, University of California, Irvine, CA, and approved April 18, 2013 (received for review February 13, 2013) Neocortical development in humans is characterized by an ex- humans only ∼25% of adult mass is achieved at birth (8). Con- tended period of synaptic proliferation that peaks in mid-child- comitantly, the postnatal refinement of cortical microstructure in hood, with subsequent pruning through early adulthood, as well humans progresses along a more protracted schedule relative to as relatively delayed maturation of neuronal arborization in the macaques.
    [Show full text]
  • Multiple Periods of Functional Ocular Dominance Plasticity in Mouse Visual Cortex
    ARTICLES Multiple periods of functional ocular dominance plasticity in mouse visual cortex Yoshiaki Tagawa1,2,3, Patrick O Kanold1,3, Marta Majdan1 & Carla J Shatz1 The precise period when experience shapes neural circuits in the mouse visual system is unknown. We used Arc induction to monitor the functional pattern of ipsilateral eye representation in cortex during normal development and after visual deprivation. After monocular deprivation during the critical period, Arc induction reflects ocular dominance (OD) shifts within the binocular zone. Arc induction also reports faithfully expected OD shifts in cat. Shifts towards the open eye and weakening of the deprived eye were seen in layer 4 after the critical period ends and also before it begins. These shifts include an unexpected spatial expansion of Arc induction into the monocular zone. However, this plasticity is not present in adult layer 6. Thus, functionally assessed OD can be altered in cortex by ocular imbalances substantially earlier and far later than expected. http://www.nature.com/natureneuroscience Sensory experience can modify structural and functional connectiv- been studied extensively. Here, a functional technique based on in situ ity in cortex1,2. Many previous studies of highly binocular animals hybridization for the immediate early gene Arc16 is used to investigate have led to the current consensus that visual experience is required for pathways representing the ipsilateral eye in developing and adult mouse maintenance of precise connections in the developing visual cortex and visual cortex and after visual deprivation. We find multiple periods of that competition-based mechanisms underlie ocular dominance (OD) susceptibility to visual deprivation in mouse visual cortex.
    [Show full text]
  • 1.32 Neural Computation Theories of Learning
    1.32 Neural Computation Theories of Learningq Samat Moldakarimov and Terrence J Sejnowski, University of California – San Diego, La Jolla, CA, United States; and Salk Institute for Biological Studies, La Jolla, CA, United States Ó 2017 Elsevier Ltd. All rights reserved. 1.32.1 Introduction 579 1.32.2 Hebbian Learning 580 1.32.3 Unsupervised Learning 581 1.32.4 Supervised Learning 581 1.32.5 Reinforcement Learning 583 1.32.6 Spike Timing–Dependent Plasticity 584 1.32.7 Plasticity of Intrinsic Excitability 586 1.32.8 Homeostatic Plasticity 586 1.32.9 Complexity of Learning 587 1.32.10 Conclusions 588 References 588 1.32.1 Introduction The anatomical discoveries in the 19th century and the physiological studies in the 20th century showed that the brain was made of networks of neurons connected together through synapses (Kandel et al., 2012). These discoveries led to a theory that learning could be the consequence of changes in the strengths of the synapses (Hebb, 1949). The Hebb’s rule for synaptic plasticity states that: When an axon of cell A is near enough to excite cell B and repeatedly or persistently takes part in firing it, some growth process or metabolic change takes place in one or both cells such that A’sefficiency, as one of the cells firing B, is increased. Hebb (1949). This postulate was experimentally confirmed in the hippocampus, where high-frequency stimulation (HFS) of a presynaptic neuron causes long-term potentiation (LTP) in the synapses connecting it to the postsynaptic neurons (Bliss and Lomo, 1973). LTP takes place only if the postsynaptic cell is also active and sufficiently depolarized (Kelso et al., 1986).
    [Show full text]
  • The Plasticity-Pathology Continuum: Defining a Role for the LTP
    Journal of Neuroscience Research 58:42–61 (1999) The Plasticity–Pathology Continuum: Defining a Role for the LTP Phenomenon Jill C. McEachern1* and Christopher A. Shaw1,2 1Department of Physiology, University of British Columbia, Vancouver, Canada 2Departments of Ophthalmology and Neuroscience, University of British Columbia, Vancouver, Canada Long-term potentiation (LTP) is the most widely Key words: homeostasis; receptor regulation; kin- studied form of neuroplasticity and is believed by dling; age-dependence; neuroplasticity many in the field to be the substrate for learning and memory. For this reason, an understanding of the INTRODUCTION mechanisms underlying LTP is thought to be of fundamental importance to the neurosciences, but a Since its discovery by Bliss and Lomo (1973), the definitive linkage of LTP to learning or memory has phenomenon of long-term potentiation (LTP) has domi- not been achieved. Much of the correlational data nated the empirical and theoretical search for the synaptic/ used to support this claim is ambiguous and controver- cellular basis of learning and memory. Many thousands of sial, precluding any solid conclusion about the func- articles and chapters have been written about the diverse tional relevance of this often artificially induced form subtypes of the phenomenon and the myriad characteris- tics that describe it (for references, see McEachern and of neuroplasticity. In spite of this fact, the belief that Shaw, 1996a,b). Synaptic potentiations that appear to be LTP is a mechanism subserving learning and/or LTP-like have been identified in every imaginable neural memory has become so dominant in the field that the circuit and subpopulation of both vertebrates and inverte- investigation of other potential roles or actions of brates.
    [Show full text]
  • Synaptic Plasticity and Addiction 2007
    REVIEWS Synaptic plasticity and addiction Julie A. Kauer* and Robert C. Malenka‡ Abstract | Addiction is caused, in part, by powerful and long-lasting memories of the drug experience. Relapse caused by exposure to cues associated with the drug experience is a major clinical problem that contributes to the persistence of addiction. Here we present the accumulated evidence that drugs of abuse can hijack synaptic plasticity mechanisms in key brain circuits, most importantly in the mesolimbic dopamine system, which is central to reward processing in the brain. Reversing or preventing these drug-induced synaptic modifications may prove beneficial in the treatment of one of society’s most intractable health problems. Long-term potentiation More than a century ago, Ramon y Cajal speculated that Addiction is not triggered instantaneously upon (LTP). Activity-dependent information storage in the brain results from alterations exposure to drugs of abuse. It involves multiple, com- strengthening of synaptic in synaptic connections between neurons1. The discov- plex neural adaptations that develop with different transmission that lasts at least ery in 1973 of long-term potentiation (LTP) of glutamate time courses ranging from hours to days to months one hour. synapses in the hippocampus2 launched an exciting (BOX 1). Work to date suggests an essential role for Long-term depression exploration into the molecular basis and behavioural synaptic plasticity in the VTA in the early behavioural (LTD). Activity-dependent correlates of synaptic plasticity. Partly because LTP was responses following initial drug exposures, as well as in weakening of synaptic first described at synapses in the hippocampus, a brain triggering long-term adaptations in regions innervated transmission that lasts at least 9 one hour.
    [Show full text]
  • Neuroplasticity
    4/14/2019 Brain: Important Facts • CNS begins from 2 • Uses 20% of the body weeks gestation energy • At birth, human brain • Consume 20 % of the weighs 350 g, at 1 year body oxygen 1000 g • All parts of brain are ISTE 2012 • 10% of the cells are involved in learning, neurons (100 billion) some more than other • Each neuron makes 1,000 to 20,000 connections Copyright@ Pradip Ghosh 2019 1 Copyright@ Pradip Ghosh 2019 2 Tractography of Whole Brain Brain Growth • The number of neurons that a child is born with is largely fixed around four months before birth. • The most important mechanisms involved in the massive brain spurt that occurs in the early years of life are: – Myelination – Production of glial cells – Synaptogenesis: Formation of new synapses Copyright@ Pradip Ghosh 2019 3 Copyright@ Pradip Ghosh 2019 4 Neuroplasticity Developmental Plasticity vs Adaptive Plasticity Developmental Plasticity Adaptive Plasticity • It can be described as brain’s ability to reorganize Definition Changes in neural connections as a The brain’s ability to compensate result of interactions with the for lost functionality due to brain itself by forming new neural connections throughout environment (our experiences during damage as well as in response to the life. childhood) as a consequence of interaction with the environment developmental processes. by reorganizing its structure • Neuronal connections are continuously being created e.g. Development of visual cortex and broken and all modeled by our experiences, and Occurs in It is predetermined and occurs in Compensation for brain injury our states of health or diseases. response to response to the initial processing of and in adjustment to new sensory information by the immature experiences.
    [Show full text]
  • Cellular Mechanisms of Visual Cortical Plasticity: a Game of Cat and Mouse
    Downloaded from learnmem.cshlp.org on October 3, 2021 - Published by Cold Spring Harbor Laboratory Press REVIEW Joshua A. Gordon 1 Cellular Mechanisms of Visual Department of Physiology Cortical Plasticity: A Game of Cat Keck Center for Integrative Neuroscience and Mouse University of California San Francisco, California 94143-0444 Introduction The remarkably complex and precise pattern of connections that characterizes the mammalian visual system arises during development through the equally remarkable process of activity-dependent plasticity: Over time, the visual system learns to see. The role of activity in the development of connectivity in the visual system has been explored in detail in the primary visual cortex of cats and monkeys, where initially overlapping inputs from the two eyes segregate into ocular dominance columns during a critical period (Rakic 1976, 1977; LeVay et al. 1978, 1980). Manipulations of visual experience during this critical period have demonstrated that an activity-dependent, correlation-based competition between inputs underlies this segregation (Shatz 1990; Katz and Shatz 1996). Indeed, the correlation-based or "Hebbian" nature of this competitive plasticity underscores the similarity between the processes of development and learning (Hebb 1949; Kandel and O'Dell 1992). Although the rules governing activity-dependent development are well described, the cellular mechanisms by which patterns of neuronal activity are transduced into patterns of synaptic connectivity remain poorly understood. Cellular models of synaptic plasticity have suggested numerous candidate mechanisms, but the lack of effective and specific pharmacological tools has hindered the study of these mechanisms in plasticity in vivo. Recently, however, gene targeting techniques have enabled the generation of a large and growing number of mouse lines, each possessing specific genetic lesions (Brandon et al.
    [Show full text]
  • Changes in Plasticity Across the Lifespan: Cause of Disease and Target 4 for Intervention
    CHAPTER Changes in Plasticity Across the Lifespan: Cause of Disease and Target 4 for Intervention Lindsay Oberman, Alvaro Pascual-Leone1 Berenson-Allen Center for Noninvasive Brain Stimulation, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA, USA 1Corresponding author: Tel.: þ617-667-0203; Fax: þ617-975-5322 e-mail address: [email protected] Abstract We conceptualize brain plasticity as an intrinsic property of the nervous system enabling rapid adaptation in response to changes in an organism’s internal and external environment. In pre- natal and early postnatal development, plasticity allows for the formation of organized nervous system circuitry and the establishment of functional networks. As the individual is exposed to various sensory stimuli in the environment, brain plasticity allows for functional and structural adaptation and underlies learning and memory. We argue that the mechanisms of plasticity change over the lifespan with different slopes of change in different individuals. These changes play a key role in the clinical phenotype of neurodevelopmental disorders like autism and schizophrenia and neurodegenerative disorders such as Alzheimer’s disease. Altered plas- ticity not only can trigger maladaptive cascades and can be the cause of deficits and disability but also offers opportunities for novel therapeutic interventions. In this chapter, we discuss the importance of brain plasticity across the lifespan and how neuroplasticity-based therapies offer promise for disorders with otherwise
    [Show full text]
  • Biocultural Orchestration of Developmental Plasticity Across Levels: the Interplay of Biology and Culture in Shaping the Mind and Behavior Across the Life Span
    Psychological Bulletin Copyright 2003 by the American Psychological Association, Inc. 2003, Vol. 129, No. 2, 171–194 0033-2909/03/$12.00 DOI: 10.1037/0033-2909.129.2.171 Biocultural Orchestration of Developmental Plasticity Across Levels: The Interplay of Biology and Culture in Shaping the Mind and Behavior Across the Life Span Shu-Chen Li Max Planck Institute for Human Development The author reviews reemerging coconstructive conceptions of development and recent empirical findings of developmental plasticity at different levels spanning several fields of developmental and life sciences. A cross-level dynamic biocultural coconstructive framework is endorsed to understand cognitive and behavioral development across the life span. This framework integrates main conceptions of earlier views into a unifying frame, viewing the dynamics of life span development as occurring simultaneously within different time scales (i.e., moment-to-moment microgenesis, life span ontogeny, and human phylogeny) and encompassing multiple levels (i.e., neurobiological, cognitive, behavioral, and sociocultural). Viewed through this metatheoretical framework, new insights of potential interfaces for reciprocal cultural and experiential influences to be integrated with behavioral genetics and cognitive neuroscience research can be more easily prescribed. Metaphorically speaking, two related pendulums, one swinging concerted biological and cultural influences (hence, biocultural back and forth from nature to nurture and the other from brain to coconstructivism) in
    [Show full text]
  • Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex
    The Journal of Neuroscience, November 1, 1997, 17(21):8376–8390 Activity-Dependent Regulation of NMDAR1 Immunoreactivity in the Developing Visual Cortex Susan M. Catalano, Catherine K. Chang, and Carla J. Shatz Howard Hughes Medical Institute and Department of Molecular and Cell Biology, University of California, Berkeley, California 94720 NMDA receptors have been implicated in activity-dependent NMDAR1 immunoreactivity in layer 4 of the columns of the synaptic plasticity in the developing visual cortex. We examined blocked eye. Thus, high levels of NMDAR1 immunostaining the distribution of immunocytochemically detectable NMDAR1 within the visual cortex are temporally correlated with ocular in visual cortex of cats and ferrets from late embryonic ages to dominance column formation and developmental plasticity; the adulthood. Cortical neurons are initially highly immunostained. persistence of staining in layers 2/3 also correlates with the This level declines gradually over development, with the nota- physiological plasticity present in these layers in the adult. In ble exception of cortical layers 2/3, where levels of NMDAR1 addition, visual experience is not required for the developmen- immunostaining remain high into adulthood. Within layer 4, the tal changes in the laminar pattern of NMDAR1 levels, but the decline in NMDAR1 immunostaining to adult levels coincides presence of high levels of NMDAR1 in layer 4 during the critical with the completion of ocular dominance column formation and period does require retinal activity. These observations are the end of the critical period for layer 4. To determine whether consistent with a central role for NMDA receptors in promoting NMDAR1 immunoreactivity is regulated by retinal activity, ani- and ultimately limiting synaptic rearrangements in the develop- mals were dark-reared or retinal activity was completely ing neocortex.
    [Show full text]