Showing papers on "Developmental plasticity published in 2012"
TL;DR: A broader view of plasticity is summarized, including the forms and cellular mechanisms for the spike-timing dependence of Plasticity, and, the evidence that spike timing is an important determinant of plasticsity in vivo is summarized.
755 citations
TL;DR: The roles of spontaneous neural activity and molecular signaling in innate, experience-independent development have been clarified, as have the later roles of visual experience.
557 citations
TL;DR: It is proposed that the different forms of plasticity in the granular layer and the molecular layer operate synergistically in a temporally and spatially distributed manner, so as to ultimately create optimal output for behaviour.
Abstract: Studies on synaptic plasticity in the context of learning have been dominated by the view that a single, particular type of plasticity forms the underlying mechanism for a particular type of learning. However, emerging evidence shows that many forms of synaptic and intrinsic plasticity at different sites are induced conjunctively during procedural memory formation in the cerebellum. Here, we review the main forms of long-term plasticity in the cerebellar cortex that underlie motor learning. We propose that the different forms of plasticity in the granular layer and the molecular layer operate synergistically in a temporally and spatially distributed manner, so as to ultimately create optimal output for behaviour.
440 citations
TL;DR: It is shown that plasticity in the visual cortex is present well before, and long after, the peak of the critical period and described the established mechanisms and point out where more experimental work is needed.
Abstract: In many regions of the developing brain, neuronal circuits undergo defined phases of enhanced plasticity, termed critical periods. Work in the rodent visual cortex has led to important insights into the cellular and molecular mechanisms regulating the timing of the critical period. Although there is little doubt that the maturation of specific inhibitory circuits plays a key role in the opening of the critical period in the visual cortex, it is less clear what puts an end to it. In this review, we describe the established mechanisms and point out where more experimental work is needed. We also show that plasticity in the visual cortex is present well before, and long after, the peak of the critical period.
354 citations
TL;DR: GAs are a family of tetracyclic diterpenoid plant hormones that stimulate plant growth and developmental transitions as discussed by the authors, and they regulate developmental responses to diverse environmental stimuli.
Abstract: GAs are a family of tetracyclic diterpenoid plant hormones that stimulate plant growth and developmental transitions. As sessile organisms, plants rely on developmental plasticity to respond to environmental challenges. Plant hormones regulate developmental responses to diverse environmental stimuli
218 citations
TL;DR: It is proposed that in the adult visual cortex the experience-induced loss of inhibition may effectively strengthen specific visual inputs with limited need for rearranging the excitatory circuitry.
204 citations
TL;DR: A “phenotype-first” model of the evolution of human life history is proposed, in which novel phenotypes were first generated by behaviorally or environmentally driven plasticity and were later gradually stabilized into species-defining traits through genetic accommodation.
Abstract: The life history of Homo sapiens is characterized by a lengthy period of juvenile dependence that requires extensive allocare, short interbirth intervals with concomitantly high fertility rates, and a life span much longer than that of other extant great apes. Although recognized as species-defining, the traits that make up human life history are also notable for their extensive within- and between-population variation, which appears to trace largely to phenotypic and developmental plasticity. In this review, we first discuss the adaptive origins of plasticity in life history strategy and its influence on traits such as growth rate, maturational tempo, reproductive scheduling, and life span in modern human populations. Second, we consider the likely contributions of this plasticity to evolutionary diversification and speciation within genus Homo. Contrary to traditional assumptions that plasticity slows the pace of genetic adaptation, current empirical work and theory point to the potential for plasticity...
184 citations
TL;DR: The visual cortex has the capacity for experience-dependent change, or cortical plasticity, that is retained throughout life, and changes observed in primary visual cortex (V1) may be representative of how learned information is encoded throughout the cerebral cortex.
165 citations
TL;DR: This review describes the primary properties of CaN and illustrates its functions and modes of action by focusing on several representative targets, in particular glutamate receptors, striatal enriched protein phosphatase (STEP), and neuromodulin (GAP43), and their functional significance for synaptic plasticity and memory.
Abstract: Major brain functions depend on neuronal processes that favor the plasticity of neuronal circuits while at the same time maintaining their stability. The mechanisms that regulate brain plasticity are complex and engage multiple cascades of molecular components that modulate synaptic efficacy. Protein kinases (PKs) and phosphatases (PPs) are among the most important of these components that act as positive and negative regulators of neuronal signaling and plasticity, respectively. In these cascades, the PP protein phosphatase 2B or calcineurin (CaN) is of particular interest because it is the only Ca(2+)-activated PP in the brain and a major regulator of key proteins essential for synaptic transmission and neuronal excitability. This review describes the primary properties of CaN and illustrates its functions and modes of action by focusing on several representative targets, in particular glutamate receptors, striatal enriched protein phosphatase (STEP), and neuromodulin (GAP43), and their functional significance for synaptic plasticity and memory.
151 citations
TL;DR: A transition between homeostatic and long-term potentiation–like plasticity mechanisms with increasing age is revealed, which concludes that increased responsiveness to open-eye stimulation after monocular deprivation during the critical period is aHomeostatic process that depends mechanistically on synaptic scaling during thecritical period, whereas in adult mice it is mediated by a different mechanism that requires αCaMKII autophosphorylation.
Abstract: Ocular dominance (OD) plasticity in the visual cortex is a classic model system for understanding developmental plasticity, but the visual cortex also shows plasticity in adulthood. Whether the plasticity mechanisms are similar or different at the two ages is not clear. Several plasticity mechanisms operate during development, including homeostatic plasticity, which acts to maintain the total excitatory drive to a neuron. In agreement with this idea, we found that an often-studied substrain of C57BL/6 mice, C57BL/6JOlaHsd (6JOla), lacks both the homeostatic component of OD plasticity as assessed by intrinsic signal imaging and synaptic scaling of mEPSC amplitudes after a short period of dark exposure during the critical period, whereas another substrain, C57BL/6J (6J), exhibits both plasticity processes. However, in adult mice, OD plasticity was identical in the 6JOla and 6J substrains, suggesting that adult plasticity occurs by a different mechanism. Consistent with this interpretation, adult OD plasticity was normal in TNFα knockout mice, which are known to lack juvenile synaptic scaling and the homeostatic component of OD plasticity, but was absent in adult α-calcium/calmodulin-dependent protein kinase II;T286A (αCaMKIIT286A) mice, which have a point mutation that prevents autophosphorylation of αCaMKII. We conclude that increased responsiveness to open-eye stimulation after monocular deprivation during the critical period is a homeostatic process that depends mechanistically on synaptic scaling during the critical period, whereas in adult mice it is mediated by a different mechanism that requires αCaMKII autophosphorylation. Thus, our study reveals a transition between homeostatic and long-term potentiation–like plasticity mechanisms with increasing age.
134 citations
TL;DR: This work focuses on how myelin associated inhibitors limit a wide spectrum of growth that includes regeneration, sprouting, and plasticity in both the intact and lesioned CNS.
TL;DR: It is shown, using lactation to repeatedly activate a specific endocrine cell network in situ in the mammalian pituitary, that templates of prior demand are permanently stored through stimulus-evoked alterations to the extent and strength of cell–cell connectivity.
Abstract: Experience-dependent plasticity of cell and tissue function is critical for survival by allowing organisms to dynamically adjust physiological processes in response to changing or harsh environmental conditions. Despite the conferred evolutionary advantage, it remains unknown whether emergent experience-dependent properties are present in cell populations organized as networks within endocrine tissues involved in regulating body-wide homeostasis. Here we show, using lactation to repeatedly activate a specific endocrine cell network in situ in the mammalian pituitary, that templates of prior demand are permanently stored through stimulus-evoked alterations to the extent and strength of cell-cell connectivity. Strikingly, following repeat stimulation, evolved population behaviour leads to improved tissue output. As such, long-lasting experience-dependent plasticity is an important feature of endocrine cell networks and underlies functional adaptation of hormone release.
TL;DR: It is suggested that polymorphic variation at the oxytocin receptor gene is associated with sociability, amygdala volume and differential risk for psychiatric conditions including autism, depression and anxiety disorder, depending on the quality of early environmental experiences.
Abstract: The diathesis-stress model of psychiatric conditions has recently been challenged by the view that it might be more accurate to speak of 'differential susceptibility' or 'plasticity' genes, rather than one-sidedly focusing on individual vulnerability. That is, the same allelic variation that predisposes to a psychiatric disorder if associated with (developmentally early) environmental adversity may lead to a better-than-average functional outcome in the same domain under thriving (or favourable) environmental conditions. Studies of polymorphic variations of the serotonin transporter gene, the monoamino-oxidase-inhibitor A coding gene or the dopamine D4 receptor gene indicate that the early environment plays a crucial role in the development of favourable versus unfavourable outcomes. Current evidence is limited, however, to establishing a link between genetic variation and behavioural phenotypes. In contrast, little is known about how plasticity may be expressed at the neuroanatomical level as a 'hard-wired' correlate of observable behaviour. The present review article seeks to further strengthen the argument in favour of the differential susceptibility theory by incorporating findings from behavioural and neuroanatomical studies in relation to genetic variation of the oxytocin receptor gene. It is suggested that polymorphic variation at the oxytocin receptor gene (rs2254298) is associated with sociability, amygdala volume and differential risk for psychiatric conditions including autism, depression and anxiety disorder, depending on the quality of early environmental experiences. Seeing genetic variation at the core of developmental plasticity can explain, in contrast to the diathesis-stress perspective, why evolution by natural selection has maintained such 'risk' alleles in the gene pool of a population.
TL;DR: In this paper, the authors explored the degree of behavioural plasticity versus personality in the bridge spider, Larinioides sclopetarius, which occurs in extremely high densities in urban areas over the Holarctic.
TL;DR: A new model is proposed in which map expansion provides a form of replication with variation that supports a Darwinian mechanism to select the most behaviorally useful circuits.
TL;DR: Inhibitory synapse function displays a protracted development during which deficits can be induced by juvenile, but not adult, hearing loss, and these long-lasting changes to inhibitory function may contribute to the auditory processing deficits associated with early hearing loss.
Abstract: The developmental plasticity of excitatory synapses is well established, particularly as a function of age. If similar principles apply to inhibitory synapses, then we would expect manipulations during juvenile development to produce a greater effect and experience-dependent changes to persist into adulthood. In this study, we first characterized the maturation of cortical inhibitory synapse function from just before the onset of hearing through adulthood. We then examined the long-term effects of developmental conductive hearing loss (CHL). Whole cell recordings from gerbil thalamocortical brain slices revealed a significant decrease in the decay time of inhibitory currents during the first 3 mo of normal development. When assessed in adults, developmental CHL led to an enduring decrease of inhibitory synaptic strength, whereas the maturation of synaptic decay time was only delayed. Early CHL also depressed the maximum discharge rate of fast-spiking, but not low-threshold-spiking, inhibitory interneurons. We then asked whether adult onset CHL had a similar effect, but neither inhibitory current amplitude nor decay time was altered. Thus inhibitory synapse function displays a protracted development during which deficits can be induced by juvenile, but not adult, hearing loss. These long-lasting changes to inhibitory function may contribute to the auditory processing deficits associated with early hearing loss.
TL;DR: These studies demonstrate the major functional partition of plasticity within a single cortical layer and reveal the LII/III to LV connection as a major excitatory locus of cortical plasticity.
TL;DR: It is demonstrated that highland deer mice have enhanced thermogenic capacities under hypoxia, and that performance differences between highland and lowland mice persist when individuals are born and reared under common-garden conditions, suggesting that differences in thermogenic capacity have a genetic basis.
Abstract: Small mammals face especially severe thermoregulatory challenges at high altitude because the reduced O2 availability constrains the capacity for aerobic thermogenesis. Adaptive enhancement of thermogenic performance under hypoxic conditions may be achieved via physiological adjustments that occur within the lifetime of individuals (phenotypic plasticity) and/or genetically based changes that occur across generations, but their relative contributions to performance differences between highland and lowland natives are unclear. Here, we examined potentially evolved differences in thermogenic performance between populations of deer mice ( Peromyscus maniculatus ) that are native to different altitudes. The purpose of the study was to assess the contribution of phenotypic plasticity to population differences in thermogenic performance under hypoxia. We used a common-garden deacclimation experiment to demonstrate that highland deer mice have enhanced thermogenic capacities under hypoxia, and that performance differences between highland and lowland mice persist when individuals are born and reared under common-garden conditions, suggesting that differences in thermogenic capacity have a genetic basis. Conversely, population differences in thermogenic endurance appear to be entirely attributable to physiological plasticity during adulthood. These combined results reveal distinct sources of phenotypic plasticity for different aspects of thermogenic performance, and suggest that thermogenic capacity and endurance may have different mechanistic underpinnings.
TL;DR: It is determined that unless a minimum of four pluripotent cells is established before implantation, development will arrest, and this failure can be rescued by modulating Fgf and Wnt signaling to enhance pluripotency, allowing the generation of monozygotic twins, which is an otherwise rare phenomenon.
TL;DR: A form of activity-dependent plasticity that is somewhat unique to GABAergic transmission is examined, which involves short-lasting changes to the ionic driving force for the post-synaptic receptors, a process referred to as short-term ionic plasticity.
Abstract: Fast synaptic inhibition in the brain is mediated by the pre-synaptic release of the neurotransmitter γ-Aminobutyric acid (GABA)and the post-synaptic activation of GABA-sensitive ionotropic receptors. As with excitatory synapses, it is being increasinly appreciated that a variety of plastic processes occur at inhibitory synapses, which operate over a range of timescales. Here we examine a form of activity-dependent plasticity that is somewhat unique to GABAergic transmission. This involves short-lasting changes to the ionic driving force for the post-synaptic receptors, a process referred to as short-term ionic plasticity. These changes are directly related to the history of activity at inhibitory synapses and are influenced by a variety of factors including the location of the synapse and the post-synaptic cell's ion regulation mechanisms. We explore the processes underlying this form of plasticity, when and where it can occur, and how it is likely to impact network activity.
TL;DR: It is found that the two main types of adult-born neurons in the mouse olfactory bulb undergo experience-dependent plasticity long after maturation and integration, as evidenced by stabilization of synaptic turnover rates.
Abstract: The adult olfactory bulb and hippocampus are continuously supplied with newborn neurons that are thought to possess a capacity for plasticity only at a young neuronal age, mainly during the early stages of integration into the network. We find that the two main types of adult-born neurons in the mouse olfactory bulb undergo experience-dependent plasticity long after maturation and integration, as evidenced by stabilization of synaptic turnover rates. Thus, the potential time window for plasticity of adult-born neurons extends well into maturity.
TL;DR: Exogenous administration of IGF-1 in the adult visual cortex restores the susceptibility of cortical neurons to monocular deprivation and promotes the recovery of normal visual functions in adult amblyopic animals.
Abstract: The central nervous system architecture is markedly modified by sensory experience during early life, but a decline of plasticity occurs with age. Recent studies have challenged this dogma providing evidence that both pharmacological treatments and paradigms based on the manipulation of environmental stimulation levels can be successfully employed as strategies for enhancing plasticity in the adult nervous system. Insulin-like growth factor 1 (IGF-1) is a peptide implicated in prenatal and postnatal phases of brain development such as neurogenesis, neuronal differentiation, synaptogenesis, and experience-dependent plasticity. Here, using the visual system as a paradigmatic model, we report that IGF-1 reactivates neural plasticity in the adult brain. Exogenous administration of IGF-1 in the adult visual cortex, indeed, restores the susceptibility of cortical neurons to monocular deprivation and promotes the recovery of normal visual functions in adult amblyopic animals. These effects were accompanied by a marked reduction of intracortical GABA levels. Moreover, we show that a transitory increase of IGF-1 expression is associated to the plasticity reinstatement induced by environmental enrichment (EE) and that blocking IGF-1 action by means of the IGF-1 receptor antagonist JB1 prevents EE effects on plasticity processes.
TL;DR: The findings indicate that in addition to their role in modifying sensory processing, mechanisms of attention can also be a potent modulator of cortical plasticity.
Abstract: Neural plasticity plays a critical role in learning, memory, and recovery from injury to the nervous system. Although much is known about the physical and physiological determinants of plasticity, little is known about the influence of cognitive factors. In this study, we investigated whether selective attention plays a role in modifying changes in neural excitability reflecting long-term potentiation (LTP)-like plasticity. We induced LTP-like effects in the hand area of the human motor cortex using transcranial magnetic stimulation (TMS). During the induction of plasticity, participants engaged in a visual detection task with either low or high attentional demands. Changes in neural excitability were assessed by measuring motor-evoked potentials in a small hand muscle before and after the TMS procedures. In separate experiments plasticity was induced either by paired associative stimulation (PAS) or intermittent theta-burst stimulation (iTBS). Because these procedures induce different forms of LTP-like effects, they allowed us to investigate the generality of any attentional influence on plasticity. In both experiments reliable changes in motor cortex excitability were evident under low-load conditions, but this effect was eliminated under high-attentional load. In a third experiment we investigated whether the attentional task was associated with ongoing changes in the excitability of motor cortex, but found no difference in evoked potentials across the levels of attentional load. Our findings indicate that in addition to their role in modifying sensory processing, mechanisms of attention can also be a potent modulator of cortical plasticity.
TL;DR: Current evidence indicates that lifelong addition of new hippocampal neurons may extend early developmental plasticity to adulthood, which continuously rejuvenates adult brain.
Abstract: Plasticity in the adult brain enables lifelong learning. The fundamental mechanism of adult neural plasticity is activity-dependent reorganization of pre-existing structure, in contrast to the widespread cellular proliferation and migration that occurs during development. Whereas adult hippocampal dentate gyrus continuously generates cohorts of neurons, and newborn neurons integrate into the existing neural circuit under the regulation of existing global and local neural activity, demonstrating a unique cellular and synaptic flexibility in adult brain. Exhibiting an enhanced structural and synaptic plasticity during the maturation, adult-born hippocampal neurons may represent a unique population for hippocampal function. Current evidence indicates that lifelong addition of new hippocampal neurons may extend early developmental plasticity to adulthood, which continuously rejuvenates adult brain. We reviewed most recent advancements in exploring the circuit and behavioral role of adult-born hippocampal neurons.
TL;DR: The results suggest that perceptual learning and video game play may be effective in improving a range of visual performance measures and importantly the improvements may transfer to better visual acuity and stereopsis.
Abstract: Experience-dependent plasticity is closely linked with the development of sensory function. Beyond this sensitive period, developmental plasticity is actively limited; however, new studies provide growing evidence for plasticity in the adult visual system. The amblyopic visual system is an excellent model for examining the “brakes” that limit recovery of function beyond the critical period. While amblyopia can often be reversed when treated early, conventional treatment is generally not undertaken in older children and adults. However new clinical and experimental studies in both animals and humans provide evidence for neural plasticity beyond the critical period. The results suggest that perceptual learning and video game play may be effective in improving a range of visual performance measures and importantly the improvements may transfer to better visual acuity and stereopsis. These findings, along with the results of new clinical trials, suggest that it might be time to re-consider our notions about neural plasticity in amblyopia.
TL;DR: Developmental programming is potentially reversible by manipulating the concentration of circulating leptin during a critical window of developmental plasticity and offers an exciting new approach for therapeutic intervention.
TL;DR: In adult mouse brain experience-dependent plasticity is in part supported by the activity of matrix metalloproteinase 9 (MMP-9), an enzyme implicated in plastic modification of the neuronal connections.
Abstract: Modifications of properties of the adult sensory cortex by elimination of sensory input (deprivation) serves as a model for studying plasticity in the adult brain. We studied the effects of short- and long-term deprivation (sparing one row of vibrissae) upon the barrel cortex. The response to stimulation (exploration of a new environment) of the spared row was examined with [14C]-2-deoxyglucose autoradiography and c-Fos immunohistochemistry. Both methods found large increases of the functional cortical representation of the spared row of vibrissae, extending into parts of the barrel cortex previously activated by the deprived vibrissae. With both methods, the greatest expansion of spared input was observed in cortical layer IV. In this way, we established a model, which was applied for examining involvement of matrix metalloproteinase 9 (MMP-9), upon experience-dependent cortical plasticity. MMP-9 is an enzyme implicated in plastic modification of the neuronal connections. We found that MMP-9 activity was increased in response to stimulation, and furthermore, MMP-9 knockout mice showed a modest but significant decrease of plasticity in layer IV with 2-DG mapping and in layers II/III with c-Fos mapping. Thus, in adult mouse brain experience-dependent plasticity is in part supported by the activity of MMP-9.
TL;DR: This review will focus on critical windows of development and possible therapeutic avenues that may reduce metabolic and obesogenic risk following an adverse early life environment.
Abstract: Obesity and the metabolic syndrome have reached epidemic proportions worldwide with far-reaching health care and economic implications. The rapid increase in the prevalence of these disorders suggests that environmental and behavioral influences, rather than genetic causes, are fueling the epidemic. The developmental origins of health and disease hypothesis has highlighted the link between the periconceptual, fetal, and early infant phases of life and the subsequent development of metabolic disorders in later life. In particular, the impact of poor maternal nutrition on susceptibility to later life metabolic disease in offspring is now well documented. Several studies have now shown, at least in experimental animal models, that some components of the metabolic syndrome, induced as a consequence of developmental programming, are potentially reversible by nutritional or targeted therapeutic interventions during windows of developmental plasticity. This review will focus on critical windows of development and possible therapeutic avenues that may reduce metabolic and obesogenic risk following an adverse early life environment.
TL;DR: Flies evolved under variable environments had a greater capacity to acclimate the PE/PC ratio compared to flies evolved in constant environments, supporting the prediction that environments with high among‐generation variance favor greater developmental plasticity.
Abstract: Theory predicts that developmental plasticity, the capacity to change phenotypic trajectory during development, should evolve when the environment varies sufficiently among generations, owing to temporal (e.g., seasonal) variation or to migration among environments. We characterized the levels of cellular plasticity during development in populations of Drosophila melanogaster experimentally evolved for over three years in either constant or temporally variable thermal environments. We used two measures of the lipid composition of cell membranes as indices of physiological plasticity (a.k.a. acclimation): (1) change in the ratio of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) and (2) change in lipid saturation (number of double bonds) in cool (16°C) relative to warm (25°C) developmental conditions. Flies evolved under variable environments had a greater capacity to acclimate the PE/PC ratio compared to flies evolved in constant environments, supporting the prediction that environments with high among-generation variance favor greater developmental plasticity. Our results are consistent with the selective advantage of a more environmentally sensitive allele that may have associated costs in constant environments.
TL;DR: Overexpression of NPAS4 restores plasticity in the adult visual cortex and down‐regulation prevents the plastic outcome caused by fluoxetine in adulthood.
Abstract: There is evidence that developmental-like plasticity can be reactivated in the adult visual cortex. Although activity-dependent transcription factors underlying the process of plasticity reactivation are currently unknown, recent studies point towards NPAS4 as a candidate gene for the occurrence of plasticity in the adult visual system. Here, we addressed whether NPAS4 is involved in the reinstatement of plasticity by using the monocular deprivation protocol and long-term fluoxetine treatment as a pharmacological strategy that restores plasticity in adulthood. A combination of molecular assays for gene expression and epigenetic analysis, gene delivery by lentiviral infection, shRNA interference and electrophysiology as a functional read-out, revealed a previously unknown role for the transcription factor NPAS4 in the regulation of adult visual cortical plasticity. We found that NPAS4 overexpression restores ocular dominance plasticity in adult naive animals whereas NPAS4 down-regulation prevents the plastic outcome caused by fluoxetine in adulthood. Our findings lead the way to the identification of novel therapeutic targets for pathological conditions where reorganization of neuronal networks would be beneficial in adult life.