Developmental plasticity

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

Glial cells in synaptic plasticity.

Abstract: Plasticity of synaptic transmission is believed to be the cellular basis for learning and memory, and depends upon different pre- and post-synaptic neuronal mechanisms. Recently, however, an increasing number of studies have implicated a third element in plasticity; the perisynaptic glial cell. Originally glial cells were thought to be important for metabolic maintenance and support of the nervous system. However, work in the past decade has clearly demonstrated active involvement of glia in stability and overall nervous system function as well as synaptic plasticity. Through specific modulation of glial cell function, a wide variety of roles for glia in synaptic plasticity have been uncovered. Furthermore, interesting circumstantial evidence suggests a glial involvement in multiple other types of plasticity. We will discuss recent advances in neuron–glial interactions that take place during synaptic plasticity and explore different plasticity phenomena in which glial cells may be involved.

SYNGAP1 Links the Maturation Rate of Excitatory Synapses to the Duration of Critical-Period Synaptic Plasticity

Abstract: Critical periods of developmental plasticity contribute to the refinement of neural connections that broadly shape brain development. These windows of plasticity are thought to be important for the maturation of perception, language, and cognition. Synaptic properties in cortical regions that underlie critical periods influence the onset and duration of windows, although it remains unclear how mechanisms that shape synapse development alter critical-period properties. In this study, we demonstrate that inactivation of a single copy of syngap1, which causes a surprisingly common form of sporadic, non-syndromic intellectual disability with autism in humans, induced widespread early functional maturation of excitatory connections in the mouse neocortex. This accelerated functional maturation was observed across distinct areas and layers of neocortex and directly influenced the duration of a critical-period synaptic plasticity associated with experience-dependent refinement of cortical maps. These studies support the idea that genetic control over synapse maturation influences the duration of critical-period plasticity windows. These data also suggest that critical-period duration links synapse maturation rates to the development of intellectual ability.

Mechanisms underlying rapid experience-dependent plasticity in the human visual cortex.

Abstract: Visual deprivation induces a rapid increase in visual cortex excitability that may result in better consolidation of spatial memory in animals and in lower visual recognition thresholds in humans. gamma-Aminobutyric acid (GABA)ergic, N-methyl-d-aspartate (NMDA), and cholinergic receptors are thought to be involved in visual cortex plasticity in animal studies. Here, we used a pharmacological approach and found that lorazepam (which enhances GABA(A) receptor function by acting as a positive allosteric modulator), dextrometorphan (NMDA receptor antagonist), and scopolamine (muscarinic receptor antagonist) blocked rapid plastic changes associated with light deprivation. These findings suggest the involvement of GABA, NMDA, and cholinergic receptors in rapid experience-dependent plasticity in the human visual cortex.

A developmental morphologist's perspective on plasticity

Abstract: This series of essays addresses plasticity from the perspective of developmental morphology. The first essay deals with the problem of distinguishing between plasticity and other types of ontogenetic variation. In a temporally varying environment, morphological plasticity may be expressed as the production of a succession of different metamers. However, even in a constant environment, plant metamers can vary dramatically, a phenomenon known as heteroblasty. Because heteroblasty and plasticity can yield similar patterns of ontogenetic variation, the two are often confounded in analyses of developmental plasticity. The second essay discusses the integration of plant phenotypic responses and finds that the evidence for integration is equivocal. The third section shows that developmental properties can constrain the expression of morphological plasticity. Developmental lags and the ‘epiphenotype problem’ are particularly important features for analyses of the evolution and expression of plasticity. Finally, in answer to the question of strategies for studying plasticity, I emphasize the need for research at multiple levels and for the inclusion of a historical or phylogenetic perspective.