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: A meta-analysis of transcriptional and translational changes during altered whisker use is performed to nominate the major molecular correlates of experience-dependent map plasticity in the barrel cortex and proposes a gene regulatory network that could couple activity dependent changes in neurons to adaptive changes in neurovasculature.
26 citations
TL;DR: Surprisingly, rather than mirroring the effects of visual deprivation, mice that lack the plasticity gene Arc show increased numbers of binocular neurons and a shift in ocular dominance during development, suggesting that the maintenance ofbinocular circuits requires ongoing plasticity.
26 citations
TL;DR: How elevated θM may be related to reduced levels of neurotransmitters modulating plasticity, abnormally low expression of N-methyl-d-aspartate receptors (NMDARs), and the membrane translocation of Ca2+/calmodulin-dependent protein kinase II in adult rat cortex subjected to prenatal alcohol exposure is discussed.
Abstract: We model experience-dependent plasticity in the cortical representation of whiskers (the barrel cortex) in normal adult rats, and in adult rats that were prenatally exposed to alcohol. Prenatal exposure to alcohol (PAE) caused marked deficits in experience-dependent plasticity in a cortical barrel-column. Cortical plasticity was induced by trimming all whiskers on one side of the face except two. This manipulation produces high activity from the intact whiskers that contrasts with low activity from the cut whiskers while avoiding any nerve damage. By a computational model, we show that the evolution of neuronal responses in a single barrel-column after this sensory bias is consistent with the synaptic modifications that follow the rules of the Bienenstock, Cooper, and Munro (BCM) theory. The BCM theory postulates that a neuron possesses a moving synaptic modification threshold, θM, that dictates whether the neuron's activity at any given instant will lead to strengthening or weakening of its input synapses. The current value of θM changes proportionally to the square of the neuron's activity averaged over some recent past. In the model of alcohol impaired cortex, the effective θM has been set to a level unattainable by the depressed levels of cortical activity leading to “impaired” synaptic plasticity that is consistent with experimental findings. Based on experimental and computational results, we discuss how elevated θM may be related to (i) reduced levels of neurotransmitters modulating plasticity, (ii) abnormally low expression of N-methyl-d-aspartate receptors (NMDARs), and (iii) the membrane translocation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) in adult rat cortex subjected to prenatal alcohol exposure.
26 citations
TL;DR: The long developmental history of the P300, in contrast to the ABRs, provides a functional measure of developmental plasticity in a cognitive versus a sensory brain system.
26 citations
TL;DR: It is reported that the lineage-specific sulfotransferase SEUD-1, which responds to environmental cues, dosage-dependently regulates polyphenism of mouthparts in the nematode Pristionchus pacificus.
Abstract: Polyphenism, the extreme form of developmental plasticity, is the ability of a genotype to produce discrete morphologies matched to alternative environments. Because polyphenism is likely to be under switch-like molecular control, a comparative genetic approach could reveal the molecular targets of plasticity evolution. Here we report that the lineage-specific sulfotransferase SEUD-1, which responds to environmental cues, dosage-dependently regulates polyphenism of mouthparts in the nematode Pristionchus pacificus. SEUD-1 is expressed in cells producing dimorphic morphologies, thereby integrating an intercellular signalling mechanism at its ultimate target. Additionally, multiple alterations of seud-1 support it as a potential target for plasticity evolution. First, a recent duplication of seud-1 in a sister species reveals a direct correlation between genomic dosage and polyphenism threshold. Second, inbreeding to produce divergent polyphenism thresholds resulted in changes in transcriptional dosage of seud-1. Our study thus offers a genetic explanation for how plastic responses evolve.
25 citations