Topic
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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TL;DR: Olfactory preference learning begins in utero and continues neonatally, allowing young rats to become attracted to the odors of their mother, and this type of learning shares mechanisms both with other forms of developmental plasticity and with adult olfactory learning.
56 citations
TL;DR: A new twist to the relationship between synaptic plasticity and learning and memory is revealed by the latest series of studies comparing animal behavior with electrophysiological recordings in the hippocampus.
56 citations
TL;DR: Understanding plasticity mechanisms could have major implications in the diagnosis and treatment of ocular diseases, such as retinal disorders, cataract and refractive surgery, amblyopia, and in the evaluation of surgical materials and techniques.
Abstract: Neuroplasticity refers to the ability of the brain to reorganize the function and structure of its connections in response to changes in the environment. Adult human visual cortex shows several manifestations of plasticity, such as perceptual learning and adaptation, working under the top-down influence of attention. Plasticity results from the interplay of several mechanisms, including the GABAergic system, epigenetic factors, mitochondrial activity, and structural remodeling of synaptic connectivity. There is also a downside of plasticity, that is, maladaptive plasticity, in which there are behavioral losses resulting from plasticity changes in the human brain. Understanding plasticity mechanisms could have major implications in the diagnosis and treatment of ocular diseases, such as retinal disorders, cataract and refractive surgery, amblyopia, and in the evaluation of surgical materials and techniques. Furthermore, eliciting plasticity could open new perspectives in the development of strategies that trigger plasticity for better medical and surgical outcomes.
56 citations
TL;DR: Data support the hypothesis that excess Mauthner cells are incorporated into the escape-response circuit, but they divide their target territory to maintain a normal response, thus demonstrating plasticity in the formation of the Escape- response circuit.
Abstract: The relatively simple neural circuit driving the escape response in zebrafish offers an excellent opportunity to study properties of neural circuit formation. The hindbrain Mauthner cell is an essential component of this circuit. Mutations in the zebrafish deadly seven/notch1a (des) gene result in supernumerary Mauthner cells. We addressed whether and how these extra cells are incorporated into the escape-response circuit. Calcium imaging revealed that all Mauthner cells in desb420 mutants were active during an elicited escape response. However, the kinematic performance of the escape response in mutant larvae was very similar to wild-type fish. Analysis of the relationship between Mauthner axon collaterals and spinal neurons revealed that there was a decrease in the number of axon collaterals per Mauthner axon in mutant larvae compared with wild-type larvae, indicative of a decrease in the number of synapses formed with target spinal neurons. Moreover, we show that Mauthner axons projecting on the same side of the nervous system have primarily nonoverlapping collaterals. These data support the hypothesis that excess Mauthner cells are incorporated into the escape-response circuit, but they divide their target territory to maintain a normal response, thus demonstrating plasticity in the formation of the escape-response circuit. Such plasticity may be key to the evolution of the startle responses in mammals, which use larger populations of neurons in circuits similar to those in the fish escape response.
56 citations
TL;DR: These studies show a critical role for regulatory context in restricting plasticity, which is probably maintained by interacting transcription factor networks.
Abstract: The earliest stages of intrathymic T-cell development include not only the acquisition of T-cell characteristics but also programmed loss of potentials for B, natural killer, and dendritic cell development. Evidence from genetics and cell-transfer studies suggests an order and some components of the mechanisms involved in loss of these options, but some of the interpretations conflict. The conflicts can be resolved by a view that postulates overlapping windows of developmental opportunity and individual mechanisms regulating progression along each pathway. This view is consistent with molecular evidence for the expression patterns of positive regulators of non-T developmental pathways, SCL, PU.1 and Id2, in early thymocytes. To some extent, overexpression of such regulators redirects thymocyte development in vitro. Specific commitment functions may normally terminate this developmental plasticity. Both PU.1 overexpression and stimulation of ectopically expressed growth factor receptors can perturb T- and myeloid/dendritic-cell divergence, but only in permissive stages. A cell-line system that approximates DN3-stage thymocytes reveals that PU.1 can alter specification even in a homogeneous population. However, the response of the population to PU.1 is sharply discontinuous. These studies show a critical role for regulatory context in restricting plasticity, which is probably maintained by interacting transcription factor networks.
55 citations