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Developmental plasticity

About: Developmental plasticity is a research topic. Over the lifetime, 1721 publications have been published within this topic receiving 103438 citations.


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Journal ArticleDOI
TL;DR: Common pathways for adult plasticity suggest common mechanisms for activity-, experience-, and injury-dependent plasticity, with a focus on neural repair in stroke.
Abstract: Changes in brain circuits occur within specific paradigms of action in the adult brain. These paradigms include changes in behavioral activity patterns, alterations in environmental experience, and direct brain injury. Each of these paradigms can produce axonal sprouting, dendritic morphology changes, and alterations in synaptic connectivity. Activity-, experience-, and injury-dependent plasticity alter neuronal network function and behavioral output, and in the case of brain injury, may produce neurological recovery. The molecular substrate for adult neuronal plasticity overlaps in these three paradigms in key signaling pathways. These common pathways for adult plasticity suggest common mechanisms for activity-, experience-, and injury-dependent plasticity. These common pathways may also interact to enhance or impede each other during adult recovery of function after injury. This review focuses on common molecular changes evoked during the process of adult neuronal plasticity, with a focus on neural repair in stroke.

85 citations

Journal ArticleDOI
TL;DR: This review will focus on plasticity of intrinsic excitability as a key player in neural network function, an emerging area of research that undoubtedly will contribute a great deal to the understanding of the functionality of the nervous system.
Abstract: The nervous system faces an extremely difficult task. It must be flexible, both during development and in adult life, so that it can respond to a variety of environmental demands and produce adaptive behavior. At the same time the nervous system must be stable, so that the neural circuits that produce behavior function throughout the lifetime of the animal and that changes produced by learning endure. We are only beginning to understand how neural networks strike a balance between altering individual neurons in the name of plasticity, while maintaining long-term stability in neural system function. The balance of this plasticity and stability in neural networks undoubtedly plays a critical role in the normal functioning of the nervous system. While mechanisms of synaptic plasticity have garnered extensive study over the past three decades, it is only recently that more attention has been turned to plasticity of intrinsic excitability as a key player in neural network function. This review will focus on this emerging area of research that undoubtedly will contribute a great deal to our understanding of the functionality of the nervous system.

84 citations

Journal ArticleDOI
26 Jan 2012-Neuron
TL;DR: These studies demonstrate the major functional partition of plasticity within a single cortical layer and reveal the LII/III to LV connection as a major excitatory locus of cortical plasticity.

84 citations

Journal ArticleDOI
TL;DR: The hypothesis that alterations of structural plasticity could represent a common mechanism contributing to the cognitive and functional defects observed in diseases such as intellectual disability, autism spectrum disorders and schizophrenia is discussed.
Abstract: Synaptic plasticity mechanisms are usually discussed in terms of changes in synaptic strength. The capacity of excitatory synapses to rapidly modify the membrane expression of glutamate receptors in an activity-dependent manner plays a critical role in learning and memory processes by re-distributing activity within neuronal networks. Recent work has however also shown that functional plasticity properties are associated with a rewiring of synaptic connections and a selective stabilization of activated synapses. These structural aspects of plasticity have the potential to continuously modify the organization of synaptic networks and thereby introduce specificity in the wiring diagram of cortical circuits. Recent work has started to unravel some of the molecular mechanisms that underlie these properties of structural plasticity, highlighting an important role of signaling pathways that are also major candidates for contributing to developmental psychiatric disorders. We review here some of these recent advances and discuss the hypothesis that alterations of structural plasticity could represent a common mechanism contributing to the cognitive and functional defects observed in diseases such as intellectual disability, autism spectrum disorders and schizophrenia.

84 citations

Journal ArticleDOI
TL;DR: The concepts of phenotypic plasticity, natural selection, and evidence from animal models that early‐life events can program the activity of the neuroendocrine system are reviewed, at times altering life history patterns in an adaptive manner.
Abstract: The interaction of the genetic program with the environment shapes the development of an individual. Accumulating data from animal models indicate that prenatal and early-postnatal events (collectively called "early-life events") can initiate long-term changes in the expression of the genetic program which persist, or may only become apparent, much later in the individual's life. Researchers working with humans or animal models of human diseases often view the effects of early-life events through the lens of pathology, with a focus on whether the events increase the risk for a particular disease. Alternatively, comparative biologists often view the effects of early-life events through the lens of evolution and adaptation by natural selection; they investigate the processes by which environmental conditions present early in life may prompt the adoption of different developmental pathways leading to alternative life histories. Examples of both approaches are presented in this article. This article reviews the concepts of phenotypic plasticity, natural selection, and evidence from animal models that early-life events can program the activity of the neuroendocrine system, at times altering life history patterns in an adaptive manner. Data from seasonally breeding rodents are used to illustrate the use of maternally derived information to alter the life history of young. In several species, the maternal system transfers photoperiodic information to the young in utero. This maternally derived information alters the response of young to photoperiods encountered later and life, producing seasonally distinct life histories.

84 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202316
202244
202172
202076
201953
201864