Developmental plasticity

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

Phenotypic and Developmental Plasticity in Plants

Abstract: Plants have a remarkable ability to alter their development in response to myriad environmental cues or stress. This phenotypic plasticity allows them to continually adapt to their local environment, a necessity for plants as sessile organisms. A host of environmental cues can be interpreted by plants, including light, temperature and nutrients, and these inputs are integrated and translated into a range of developmental outputs from shoot elongation, regulation of root gravitropism, altered flowering time, growth cessation of leaves, and timing of germination. This plasticity enables growth optimisation for the local environment, allows range expansion into hetergeneous habitats, and may provide an advantage as the changing climate affects growth conditions around the globe. Using model organisms such as Arabidopsis, molecular mechanisms for plastic growth responses are becoming more defined. Studies of growth and plasticity in less-characterized species could expand our knowledge of the range of plasticity present in nature. Key Concepts: Multiple environmental signals are integrated to regulate plant development. Plasticity gives plants the ability to optimise growth in varied environments. Developmental plasticity comes from the meristem, which continuously produces organs throughout the plant life cycle. Environmental cues can lead to changes in mRNA and protein abundance or activity, or they can be stored as epigenetic changes. Roots and shoots respond to different environmental conditions but employ similar cellular processes. Plants’ ability to optimise growth for a local environment may provide an advantage as habitats are altered by the changing climate. Keywords: phenotypic plasticity; developmental plasticity; plant development; climate change; flowering time; germination; plant morphology

Tumour necrosis factor-mediated homeostatic synaptic plasticity in behavioural models: testing a role in maternal immune activation.

Abstract: The proinflammatory cytokine tumour necrosis factor-alpha (TNFα) has long been characterized for its role in the innate immune system, but more recently has been found to have a distinct role in the nervous system that does not overlap with other proinflammatory cytokines. Through regulation of neuronal glutamate and GABA receptor trafficking, TNF mediates a homeostatic form of synaptic plasticity, but plays no direct role in Hebbian forms of plasticity. As yet, there is no evidence to suggest that this adaptive plasticity plays a significant role in normal development, but it does maintain neuronal circuit function in the face of several types of disruption. This includes developmental plasticity in primary sensory cortices, as well as modulating the response to antidepressants, chronic antipsychotics and drugs of abuse. TNF is also a prominent component of the neuroinflammation occurring in most neuropathologies, but the role of TNF-mediated synaptic plasticity in this context remains to be determined. We tested this in a maternal immune activation (MIA) model of neurodevelopmental disorders. Using TNF-/- mice, we observed that TNF is not required for the expression of abnormal social or anxious behaviour in this model. This indicates that TNF does not uniquely contribute to the development of neuronal dysfunction in this model, and suggests that during neuroinflammatory events, compensation between the various proinflammatory cytokines is the norm.This article is part of the themed issue 'Integrating Hebbian and homeostatic plasticity'.

Determinants of Brain Plasticity 1

Abstract: evoked potential occurred which &dquo;recovered&dquo; in amplitude over time. In addition to changes in electrophysiological parameters, remote metabolic perturbations have been described by Baron. Following frontal cortex injury, reduced metabolic activity exists predominantly in the cerebellum contralateral to the injury. This disturbance was presumably mediated via injury to the corticopontocerebellar pathway. Although hypometabolism exists in the cerebellum, it is not clear why there are no cerebellar symptoins. It may be the case that hypometabolic dysfunction represents a different process than a frank lesion of the cerebellum.

Regional Specificity of GABAergic Regulation of Cross-Modal Plasticity in Mouse Visual Cortex after Unilateral Enucleation

Abstract: In adult mice, monocular enucleation (ME) results in an immediate deactivation of the contralateral medial monocular visual cortex An early restricted reactivation by open eye potentiation is followed by a late overt cross-modal reactivation by whiskers (Van Brussel et al, 2011) In adolescence (P45), extensive recovery of cortical activity after ME fails as a result of suppression or functional immaturity of the cross-modal mechanisms (Nys et al, 2014) Here, we show that dark exposure before ME in adulthood also prevents the late cross-modal reactivation component, thereby converting the outcome of long-term ME into a more P45-like response Because dark exposure affects GABAergic synaptic transmission in binocular V1 and the plastic immunity observed at P45 is reminiscent of the refractory period for inhibitory plasticity reported by Huang et al (2010), we molecularly examined whether GABAergic inhibition also regulates ME-induced cross-modal plasticity Comparison of the adaptation of the medial monocular and binocular cortices to long-term ME or dark exposure or a combinatorial deprivation revealed striking differences In the medial monocular cortex, cortical inhibition via the GABAA receptor α1 subunit restricts cross-modal plasticity in P45 mice but is relaxed in adults to allow the whisker-mediated reactivation In line, in vivo pharmacological activation of α1 subunit-containing GABAA receptors in adult ME mice specifically reduces the cross-modal aspect of reactivation Together with region-specific changes in glutamate acid decarboxylase (GAD) and vesicular GABA transporter expression, these findings put intracortical inhibition forward as an important regulator of the age-, experience-, and cortical region-dependent cross-modal response to unilateral visual deprivation SIGNIFICANCE STATEMENT In adult mice, vision loss through one eye instantly reduces neuronal activity in the visual cortex Strengthening of remaining eye inputs in the binocular cortex is followed by cross-modal adaptations in the monocular cortex, in which whiskers become a dominant nonvisual input source to attain extensive cortical reactivation We show that the cross-modal component does not occur in adolescence because of increased intracortical inhibition, a phenotype that was mimicked in adult enucleated mice when treated with indiplon, a GABAA receptor α1 agonist The cross-modal versus unimodal responses of the adult monocular and binocular cortices also mirror regional specificity in inhibitory alterations after visual deprivation Understanding cross-modal plasticity in response to sensory loss is essential to maximize patient susceptibility to sensory prosthetics

A new mechanism of synapse-specific neuronal plasticity.

Abstract: According to current concepts, long-term memory is based on structural-functional changes in particular synaptic connections between neurons in the brain (synapse-specific plasticity), which depend on the processes of translation and transcription. Studies on neurons in the mollusk Aplysia and the mammalian hippocampus have addressed a mechanism of synapse-specific plasticity which does not require synapse-specific molecular genetic processes. Stimulation of a synapse has been shown to lead to activation of intracellular second messengers in the synapse as well as “synaptic tagging”-the formation of mechanisms “recognizing” transcription products. In the neuron body, second messengers induce the synthesis of RNA and protein molecules which are widely distributed in neuron processes and which are inserted selectively only into stimulation-tagged synapses, evoking long-term changes in their functional and morphological characteristics. The results of our studies on common snail defensive behavior command neurons LPl1 and RPl1 suggest the existence of another mechanism controlling synapse-specific plasticity. On acquisition of sensitization, a number of second messengers and the genes controlled by them are involved in supporting the plasticity of defined synaptic inputs of these neurons in snails. The processes of induction of long-term facilitation in the sensory inputs of neurons from chemoreceptors on the head have been shown to involve cAMP and cAMP-dependent transcription factors of the immediate early gene C/EBP (CAAT/enhancer binding protein), while the mechanisms controlling the other sensory input of neurons LPl1 and RPl1-from mechanoreceptors on the head-involve protein kinase C and protein kinase C-dependent transcription factor SRF (serum response factor). The immediate early gene zif268 is involved in controlling the inputs from both chemo-and mechanoreceptors on the head. These results are regarded as experimental support for the hypothesis that the molecular mechanisms of synapse-specific plasticity during learning may form on the basis of a selective neurochemical “projection” of the synaptic connections onto defined genes in the neuron.