Showing papers on "Developmental plasticity published in 2008"
TL;DR: Greater appreciation of the convergence of mechanisms between stress, depression, and neuroplasticity is likely to lead to the identification of novel targets for more efficacious treatments.
1,601 citations
TL;DR: Current understanding of the mechanisms of the major forms of synaptic plasticity at excitatory synapses in the mammalian brain are reviewed.
1,504 citations
TL;DR: Recent studies of plants and animals show how studies of parental effects in an ecological context provide important insights into the origin and evolution of adaptation under variable environmental conditions.
Abstract: One of the outstanding challenges for evolutionary biologists is to understand how developmental plasticity can influence the evolutionary process. Developmental plasticity frequently involves parental effects, which might enable adaptive and context-dependent transgenerational transmission of phenotypic strategies. However, parent-offspring conflict will frequently result in parental effects that are suboptimal for parents, offspring or both. The fitness consequences of parental effects at evolutionary equilibrium will depend on how conflicts can be resolved by modifications of developmental processes, suggesting that proximate studies of development can inform ultimate questions. Furthermore, recent studies of plants and animals show how studies of parental effects in an ecological context provide important insights into the origin and evolution of adaptation under variable environmental conditions.
543 citations
TL;DR: Cellular profiling of five Arabidopsis root cell types in response to an influx of a critical resource, nitrogen, is used to uncover a vast and predominantly cell-specific response to nitrogen, revealing a previously cryptic component of cell- specific responses to nitrogen.
Abstract: The organs of multicellular species consist of cell types that must function together to perform specific tasks. One critical organ function is responding to internal or external change. Some cell-specific responses to changes in environmental conditions are known, but the scale of cell-specific responses within an entire organ as it perceives an environmental flux has not been well characterized in plants or any other multicellular organism. Here, we use cellular profiling of five Arabidopsis root cell types in response to an influx of a critical resource, nitrogen, to uncover a vast and predominantly cell-specific response. We show that cell-specific profiling increases sensitivity several-fold, revealing highly localized regulation of transcripts that were largely hidden from previous global analyses. The cell-specific data revealed responses that suggested a coordinated developmental response in distinct cell types or tissues. One example is the cell-specific regulation of a transcriptional circuit that we showed mediates lateral root outgrowth in response to nitrogen via microRNA167, linking small RNAs to nitrogen responses. Together, these results reveal a previously cryptic component of cell-specific responses to nitrogen. Thus, the results make an important advance in our understanding of how multicellular organisms cope with environmental change at the cell level.
532 citations
TL;DR: It is suggested that experience-dependent competition in developing visual cortex is the outcome of two distinct, noncompetitive processes, a loss of deprived-eye responses followed by an apparently homeostatic increase in responses dependent on TNFalpha signaling.
396 citations
TL;DR: When marine fish were reared on alternative diets, plasticity of head and mouth shape paralleled phenotypic divergence between the derived ecotypes, supporting the flexible stem model.
Abstract: If an ancestral stem group repeatedly colonizes similar environments, developmental plasticity specific to that group should consistently give rise to similar phenotypes. Parallel selection on those similar phenotypes could lead to the repeated evolution of characteristic ecotypes, a property common to many adaptive radiations. A key prediction of this "flexible stem" model of adaptive radiation is that patterns of phenotypic divergence in derived groups should mirror patterns of developmental plasticity in their common ancestor. The threespine stickleback radiation provides an excellent opportunity to test this prediction because the marine form is representative of the ancestral stem group, which has repeatedly given rise to several characteristic ecotypes. We examined plasticity of several aspects of shape and trophic morphology in response to diets characteristic of either the derived benthic ecotype or the limnetic ecotype. When marine fish were reared on alternative diets, plasticity of head and mouth shape paralleled phenotypic divergence between the derived ecotypes, supporting the flexible stem model. Benthic and limnetic fish exhibited patterns of plasticity similar to those of the marine population; however, some differences in population means were present, as well as subtle differences in shape plasticity in the benthic population, indicating a role for genetic accommodation in this system.
278 citations
TL;DR: Investigating differences between adult and juvenile ocular dominance plasticity using Fourier optical imaging of intrinsic signals in mouse visual cortex reveals that adult plasticity takes longer than in the juvenile mouse, is of smaller magnitude, has a greater contribution from the increase in response to the open eye, and has less effect on the hemisphere ipsilateral to the deprived eye.
Abstract: Sensory experience profoundly shapes neural circuitry of juvenile brain. Although the visual cortex of adult rodents retains a capacity for plasticity in response to monocular visual deprivation, the nature of this plasticity and the neural circuit changes that accompany it remain enigmatic. Here, we investigate differences between adult and juvenile ocular dominance plasticity using Fourier optical imaging of intrinsic signals in mouse visual cortex. This comparison reveals that adult plasticity takes longer than in the juvenile mouse, is of smaller magnitude, has a greater contribution from the increase in response to the open eye, and has less effect on the hemisphere ipsilateral to the deprived eye. Binocular deprivation also causes different changes in the adult. Adult plasticity is similar to juvenile plasticity in its dependence on signaling through NMDA receptors. We propose that adult ocular dominance plasticity arises from compensatory mechanisms that counterbalance the loss of afferent activity caused by visual deprivation.
256 citations
TL;DR: A greater understanding of developmental pathways is needed to determine whether shy/bold phenotypes per se are the sole focus of selection, as differences in developmental plasticity between shy/ Bold phenotypes may also confer differential fitness in fluctuating environments.
191 citations
TL;DR: The quality of both the pre- and post-natal developmental environment can be a significant source of variation in the responsiveness of the HPA axis, and provides a frame-work for examining ecologically-relevant sources of stress-induced programming and plasticity in this endocrine system in a free-living vertebrate, respectively.
189 citations
TL;DR: It is suggested that the human auditory system exhibits developmental plasticity, in both frequency and time domains, for sounds that are composed of acoustic elements relevant to speech.
Abstract: Development of the human auditory brainstem is thought to be primarily complete by the age of ∼2 years, such that subsequent sensory plasticity is confined primarily to the cortex. However, recent findings have revealed experience-dependent developmental plasticity in the mammalian auditory brainstem in an animal model. It is not known whether the human system demonstrates similar changes and whether experience with sounds composed of acoustic elements relevant to speech may alter brainstem response characteristics. We recorded brainstem responses evoked by both click and speech syllables in children between the ages of 3 and 12 years. Here, we report a neural response discrepancy in brainstem encoding of these two sounds, observed in 3- to 4-year-old children but not in school-age children. Whereas all children exhibited identical neural activity to a click, 3- to 4-year-old children displayed delayed and less synchronous onset and sustained neural response activity when elicited by speech compared with 5- to 12-year-olds. These results suggest that the human auditory system exhibits developmental plasticity, in both frequency and time domains, for sounds that are composed of acoustic elements relevant to speech. The findings are interpreted within the contexts of stimulus-related differences and experience-dependent plasticity.
154 citations
TL;DR: A network-level explanation as to how inhibition regulates the experience-dependent plasticity of neocortex is offered as well as a minimal linear model that reveals that the delay in inhibitory cell plasticity potently accelerates Hebbian plasticity in neighboring excitatory neurons.
Abstract: During postnatal development, altered sensory experience triggers the rapid reorganization of neuronal responses and connections in sensory neocortex. This experience-dependent plasticity is disrupted by reductions of intracortical inhibition. Little is known about how the responses of inhibitory cells themselves change during plasticity. We investigated the time course of inhibitory cell plasticity in mouse primary visual cortex by using functional two-photon microscopy with single-cell resolution and genetic identification of cell type. Initially, local inhibitory and excitatory cells had similar binocular visual response properties, both favoring the contralateral eye. After 2 days of monocular visual deprivation, excitatory cell responses shifted to favor the open eye, whereas inhibitory cells continued to respond more strongly to the deprived eye. By 4 days of deprivation, inhibitory cell responses shifted to match the faster changes in their excitatory counterparts. These findings reveal a dramatic delay in inhibitory cell plasticity. A minimal linear model reveals that the delay in inhibitory cell plasticity potently accelerates Hebbian plasticity in neighboring excitatory neurons. These findings offer a network-level explanation as to how inhibition regulates the experience-dependent plasticity of neocortex.
TL;DR: In this chapter, inhibitory plasticity is proposed as an important player in circuit refinement that can contribute both to the compensatory forms of circuit plasticity in the early stages of development and to the pathological loss of function induced by visual deprivation during the critical period.
Abstract: Proper wiring of neural circuits during development depends on both molecular cues that guide connectivity and activity-dependent mechanisms that use patterned activation to adjust the strength and number of synaptic connections. In this chapter, we discuss some of the plasticity mechanisms underlying the experience-dependent rewiring of visual cortical microcircuits focusing on layer 4 of rat primary visual cortex. The microcircuit in layer 4 has the ability to regulate its excitability by shifting the balance between excitatory and inhibitory synaptic transmission in an experience-dependent manner. Early in postnatal development (shortly after eye opening), visual deprivation activates several forms of homeostatic plasticity that cooperate to adjust layer 4 excitability to compensate for reduced sensory drive. In contrast, during the classical sensitive period for rodent visual system plasticity, this homeostatic response is replaced by mechanisms that reduce the responsiveness of deprived cortex. We discuss this developmentally regulated switch in plasticity within layer 4 and how this might depend on the maturation of excitatory and inhibitory monosynaptic connections. Based on our published data, we propose inhibitory plasticity as an important player in circuit refinement that can contribute both to the compensatory forms of circuit plasticity in the early stages of development and to the pathological loss of function induced by visual deprivation during the critical period.
TL;DR: In this paper, the authors discuss the contribution of ECM molecules to different forms of plasticity, including developmental plasticity in the cortex, long-term potentiation and depression in the hippocampus, homeostatic scaling of synaptic transmission and metaplasticity.
Abstract: Extracellular matrix (ECM) in the brain is composed of molecules synthesized and secreted by neurons and glial cells in a cell-type-specific and activity-dependent manner. During development, ECM plays crucial roles in proliferation, migration and differentiation of neural cells. In the mature brain, ECM undergoes a slow turnover and supports multiple physiological processes, while restraining structural plasticity. In the first part of this review, we discuss the contribution of ECM molecules to different forms of plasticity, including developmental plasticity in the cortex, long-term potentiation and depression in the hippocampus, homeostatic scaling of synaptic transmission and metaplasticity. In the second part, we focus on pathological changes associated with epileptogenic mutations in ECM-related molecules or caused by seizure-induced remodeling of ECM. The available data suggest that ECM components regulating physiological plasticity are also engaged in different aspects of epileptogenesis, such as dysregulation of excitatory and inhibitory neurotransmission, sprouting of mossy fibers, granule cell dispersion and gliosis. At the end, we discuss combinatorial approaches that might be used to counteract seizure-induced dysregulation of both ECM molecules and extracellular proteases. By restraining ECM modification and preserving the status quo in the brain, these treatments might prove to be valid therapeutic interventions to antagonize the progression of epileptogenesis.
TL;DR: How environmental cues orientate the reproductive mode of aphids from signal perception to endocrine regulation is discussed, and a comparative analysis of sexual and asexual gametogenesis and embryogenesis is proposed, which has been possible due to the development of molecular methods.
TL;DR: Most traits showed substantial plasticity in response to the rearing environment and brain size was the only trait to exhibit variation in plasticity among populations; fish of swamp origin showed no plasticity and fish of river and lake origin exhibited smaller brain size under hypoxia.
Abstract: In this study we explore the possible role of phenotypic plasticity in the process of adaptation and evolutionary change in the African cichlid Pseudocrenilabrus multicolor victoriae. Parental fish were collected from a hypoxic swamp, a lake ecotone, and a river in Uganda. Broods (F1) were split and grown under hypoxia or normoxia. We measured mor- phological parameters of the gill apparatus, structural elements surrounding the gills, brain mass, and body shape. Most traits showed substantial plasticity in response to the rearing environment. Population effects were evident for the gill ap- paratus, surrounding elements, body shape, and brain size; however, brain size was the only trait to exhibit variation in plasticity among populations; fish of swamp origin showed no plasticity and fish of river and lake origin exhibited smaller brain size under hypoxia. We interpret these patterns as consistent with genetic assimilation via canalization (brain) or via a shift in the norm of reaction (other traits).
TL;DR: It is found that several days of vision after eye opening is necessary for triggering experience-dependent plasticity, and synaptic circuits in the visual thalamus are unexpectedly malleable during a late developmental period, after the time when normal synapse elimination and pruning has occurred.
Abstract: In the mammalian visual system, sensory experience is widely thought to sculpt cortical circuits during a precise critical period. In contrast, subcortical regions, such as the thalamus, were thought to develop at earlier ages in a vision-independent manner. Recent studies at the retinogeniculate synapse, however, have demonstrated an influence of vision on the formation of synaptic circuits in the thalamus. In mice, dark rearing from birth does not alter normal developmental maturation of the connection between retina and thalamus. However, deprivation 20 d after birth [postnatal day 20 (p20)] resulted in dramatic weakening of synaptic strength and an increase in the number of retinal inputs that innervate a thalamic relay neuron. Here, by quantifying changes in synaptic strength and connectivity in response to different time windows of deprivation, we find that several days of vision after eye opening is necessary for triggering experience-dependent plasticity. Shorter periods of visual experience do not permit similar experience-dependent synaptic reorganization. Furthermore, changes in connectivity are rapidly reversible simply by restoring normal vision. However, similar plasticity did not occur when shifting the onset of deprivation to p25. Although synapses still weakened, recruitment of additional retinal inputs no longer occurred. Therefore, synaptic circuits in the visual thalamus are unexpectedly malleable during a late developmental period, after the time when normal synapse elimination and pruning has occurred. This thalamic sensitive period overlaps temporally with experience-dependent changes in the cortex, suggesting that subcortical plasticity may influence cortical responses to sensory experience.
TL;DR: Developmental plasticity may enable organisms to "fine tune" their phenotype to optimize the performance of this critical homeostatic regulatory system, but could also increase the risk of disease later in life.
Abstract: The respiratory control system exhibits considerable plasticity, similar to other regions of the nervous system. Plasticity is a persistent change in system behavior triggered by experiences such a...
TL;DR: It is suggested that a broader approach is needed because (i) evolution maximizes inclusive fitness, requiring optimization of the outcomes of the set of maternofetal dyads produced across the mother's reproductive life, and (ii) plasticity cued by early-life information operates through trade-offs among the whole suite of life-history traits.
Abstract: In a recent opinion article, Wells accepts our fundamental claim that early metabolic plasticity in humans can contribute to later disease if there is a disparity (‘mismatch’) between nutritional experience at different phases of life, but he revives a debate and about the nature and function of the cue directing such plasticity. As in that earlier exchange, Wells argues that (i) the interests of mother and offspring are distinct, (ii) the only traits of interest are nutritional and metabolic and (iii) modern humans are in some way ‘special’ because of their extended lifespan and reproductive strategy. He argues that in humans prediction has been abandoned for a backward-looking strategy that operates solely for maternal benefit. We have explained elsewhere why we do not believe this to be the case. We suggest that a broader approach is needed because (i) evolution maximizes inclusive fitness, requiring optimization of the outcomes of the set of maternofetal dyads produced across the mother's reproductive life, (ii) plasticity cued by early-life information operates through trade-offs among the whole suite of life-history traits, and it is misleading to concentrate on a single trait and (iii) as in other species, humans use the mechanisms of developmental plasticity cued by information from the past and the present to prepare for the future.
TL;DR: The results indicate that the developing limb circuitry is born from within the existing axial-based network, which acts like a functional scaffold, and that exogenous nitric oxide facilitates locomotor activity, in contrast to its inhibitory effects on swimming at earlier larval stages of development.
11 Jan 2008
TL;DR: An enabling form of visual plasticity that commences in infant rats from eye opening is reported, in which daily threshold testing of optokinetic tracking, amid otherwise normal visual experience, stimulates enduring, visual cortex-dependent enhancement of the spatial frequency threshold for tracking.
Abstract: Developmentally regulated plasticity of vision has generally been associated with "sensitive" or "critical" periods in juvenile life, wherein visual deprivation leads to loss of visual function. Here we report an enabling form of visual plasticity that commences in infant rats from eye opening, in which daily threshold testing of optokinetic tracking, amid otherwise normal visual experience, stimulates enduring, visual cortex-dependent enhancement (>60%) of the spatial frequency threshold for tracking. The perceptual ability to use spatial frequency in discriminating between moving visual stimuli is also improved by the testing experience. The capacity for inducing enhancement is transitory and effectively limited to infancy; however, enhanced responses are not consolidated and maintained unless in-kind testing experience continues uninterrupted into juvenile life. The data show that selective visual experience from infancy can alone enable visual function. They also indicate that plasticity associated with visual deprivation may not be the only cause of developmental visual dysfunction, because we found that experientially inducing enhancement in late infancy, without subsequent reinforcement of the experience in early juvenile life, can lead to enduring loss of function.
TL;DR: Results from an overexpression/misexpression screen in Drosophila are outlined, showing that one candidate, the GSK-3β-kinase homolog, shaggy, negatively influences AP-1-dependent synaptic growth, by modulating the Jun-N-terminal kinase pathway, and also regulates presynaptic neurotransmitter release at the larval neuromuscular junction.
Abstract: AP-1, an immediate-early transcription factor comprising heterodimers of the Fos and Jun proteins, has been shown in several animal models, including Drosophila, to control neuronal development and plasticity. In spite of this important role, very little is known about additional proteins that regulate, cooperate with, or are downstream targets of AP-1 in neurons. Here, we outline results from an overexpression/misexpression screen in Drosophila to identify potential regulators of AP-1 function at third instar larval neuromuscular junction (NMJ) synapses. First, we utilize >4000 enhancer and promoter (EP) and EPgy2 lines to screen a large subset of Drosophila genes for their ability to modify an AP-1-dependent eye-growth phenotype. Of 303 initially identified genes, we use a set of selection criteria to arrive at 25 prioritized genes from the resulting collection of putative interactors. Of these, perturbations in 13 genes result in synaptic phenotypes. Finally, we show that one candidate, the GSK-3β-kinase homolog, shaggy, negatively influences AP-1-dependent synaptic growth, by modulating the Jun-N-terminal kinase pathway, and also regulates presynaptic neurotransmitter release at the larval neuromuscular junction. Other candidates identified in this screen provide a useful starting point to investigate genes that interact with AP-1 in vivo to regulate neuronal development and plasticity.
01 Jan 2008
TL;DR: This work has shown that excitatory and inhibitory synapses are subject to homeostatic regulation, and the form of plasticity present at a particular synapse likely depends on its function within a neuronal circuit.
Abstract: Homeostatic synaptic plasticity mechanisms provide a means for neurons and circuitsto maintain stable function in the face of perturbations such as developmental or activitydependent changes in synapse number or strength. These forms of plasticity use negative feedback signaling to adjust synaptic properties to keep activity close to some internal set point value. Recent work suggests that there are likely multiple forms of synaptic homeostasis, mediated by distinct signaling pathways and with distinct expression mechanisms. Both excitatory and inhibitory synapses are subject to homeostatic regulation, and the form of plasticity present at a particular synapse likely depends on its function within a neuronal circuit.
TL;DR: It is proposed that understanding the processes of epigenetic programming within the neural lineage is likely to lead to the development of more rationale strategies for cell reprogramming that may be used to expand the developmental potential of otherwise restricted progenitor populations.
Abstract: The anticipated therapeutic uses of neural stem cells depend on their ability to retain a certain level of developmental plasticity. In particular, cells must respond to developmental manipulations designed to specify precise neural fates. Studies in vivo and in vitro have shown that the developmental potential of neural progenitor cells changes and becomes progressively restricted with time. For in vitro cultured neural progenitors, it is those derived from embryonic stem cells that exhibit the greatest developmental potential. It is clear that both extrinsic and intrinsic mechanisms determine the developmental potential of neural progenitors and that epigenetic, or chromatin structural, changes regulate and coordinate hierarchical changes in fate-determining gene expression. Here, we review the temporal changes in developmental plasticity of neural progenitor cells and discuss the epigenetic mechanisms that underpin these changes. We propose that understanding the processes of epigenetic programming within the neural lineage is likely to lead to the development of more rationale strategies for cell reprogramming that may be used to expand the developmental potential of otherwise restricted progenitor populations.
TL;DR: Interestingly, the increase in undeprived ipsilateral eye responses was not correlated to the decrease in deprived contralateral eye responses, suggesting that the size of these components of OD plasticity are not genetically controlled by only a single mechanism.
Abstract: Depriving one eye of visual experience during a sensitive period of development results in a shift in ocular dominance (OD) in the primary visual cortex (V1). To assess the heritability of this form of cortical plasticity and identify the responsible gene loci, we studied the influence of monocular deprivation on OD in a large number of recombinant inbred mouse strains derived from mixed C57BL/6J and DBA/2J backgrounds (BXD). The strength of imaged intrinsic signal responses in V1 to visual stimuli was strongly heritable as were various elements of OD plasticity. This has important implications for the use of mice of mixed genetic backgrounds for studying OD plasticity. C57BL/6J showed the most significant shift in OD, while some BXD strains did not show any shift at all. Interestingly, the increase in undeprived ipsilateral eye responses was not correlated to the decrease in deprived contralateral eye responses, suggesting that the size of these components of OD plasticity are not genetically controlled by only a single mechanism. We identified a quantitative trait locus regulating the change in response to the deprived eye. The locus encompasses 13 genes, two of which--Stch and Nrip1--contain missense polymorphisms. The expression levels of Stch and to a lesser extent Nrip1 in whole brain correlate with the trait identifying them as novel candidate plasticity genes.
TL;DR: This work has shown that DNA methylation, a system of gene silencing heritable across cell divisions, may serve as a mechanism underlying the evolution of plasticity in Hymenoptera.
Abstract: Developmental plasticity can generate, from one genotype, diverse alternative phenotypes appropriate to local environmental conditions (West-Eberhard 2003). However, our understanding of the developmental-genetic mechanisms that underlie plastic responses remains incomplete. Recent research suggests that DNA methylation, a system of gene silencing heritable across cell divisions, may serve as a mechanism underlying the evolution of plasticity. In particular, several recent studies in Hymenoptera (ants, bees, wasps, and sawflies) highlight the potential importance of methylation for understanding plasticity (Wang et al. 2006; Kronforst et al. 2008; Kucharski et al. 2008).
TL;DR: The objective of the present review is to put various facets of cortical map plasticity into perspective so as to examine possible links between changes occurring at multiple scales of the neural organization of the mature brain.
TL;DR: In this novel plant–insect–fungus interaction, infection forms the cue to trade off life-history traits in order to complete development within the brief alpine summer, and creates a paradoxical negative correlation between growth rate and environmental quality.
Abstract: Adaptation to different hosts plays a central role in the evolution of specialization and speciation in phytophagous insects and parasites, and our ability to experimentally rank hosts by their quality is critical to research to understand these processes. Here we provide a counter-intuitive example in which growth is faster on poor quality hosts. The leaf beetles Oreina elongata and Oreina cacaliae share their host plant with the rust Uromyces cacaliae. Larvae reared on infected Adenostyles alliariae show reduced growth rate, reduced maximum weight and longer development time. However, they normally respond adaptively to the rust's mid-season arrival. When switched during development from healthy to infected leaves, larvae accelerate growth and reduce development time, but pupate at lower body weight. In this novel plant-insect-fungus interaction, infection forms the cue to trade off life-history traits in order to complete development within the brief alpine summer. It represents a novel mode of developmental plasticity, which is likely to be found in other host-parasite systems whenever host quality deteriorates due to multiple infection or ageing. This phenotypic plasticity would modify competition after co-infection and the mutual selection imposed by hosts and parasites, and creates a paradoxical negative correlation between growth rate and environmental quality.
TL;DR: A novel role for CRF is suggested in regulating developmental events in the hippocampus and appropriate neonatal isolation can serve to promote an endocrine state that may regulate the gradual developmental change in the induction rules for synaptic plasticity in the hippocampal CA1 region.
TL;DR: Investigation of synaptic mechanisms underlying Ocular dominance plasticity indicates that this form of plasticity is regulated by factors located at extracellular and intracellular level.
Abstract: Plasticity of cortical circuits is maximal during critical periods of postnatal development. Ocular dominance plasticity is a classical model to understand the role of experience in development of the visual cortex. Recent studies are beginning to unravel the synaptic mechanisms underlying this form of plasticity and to elucidate the different plasticity of juvenile and adult animals at mechanistic and molecular level. These investigations indicate that this form of plasticity is regulated by factors located at extracellular and intracellular level. The molecular composition of the extracellular environment in which synaptic plasticity occurs changes during development becoming less permissive for plasticity. In addition, visual experience activates epigenetic mechanisms of regulation of gene transcription that becomes downregulated in adult animals.