Showing papers on "Developmental plasticity published in 2004"

The Developmental Origins of Adult Disease

Abstract: Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders stroke, hypertension and non-insulin dependent diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging which takes account of both short and long-term outcomes.

The developmental origins of well-being.

Abstract: Low birthweight is now known to be associated with increased rates of coronary heart disease and the related disorders, stroke, hypertension and adult-onset diabetes. These associations have been extensively replicated in studies in different countries and are not the result of confounding variables. They extend across the normal range of birthweight and depend on lower birthweights in relation to the duration of gestation rather than the effects of premature birth. The associations are thought to be consequences of developmental plasticity, the phenomenon by which one genotype can give rise to a range of different physiological or morphological states in response to different environmental conditions during development. Recent observations have shown that impaired growth in infancy and rapid childhood weight gain exacerbate the effects of impaired prenatal growth. A new vision of optimal early human development is emerging, which takes account of health and well-being throughout life.

Plasticity in single neuron and circuit computations

Abstract: Plasticity in neural circuits can result from alterations in synaptic strength or connectivity, as well as from changes in the excitability of the neurons themselves. To better understand the role of plasticity in the brain, we need to establish how brain circuits work and the kinds of computations that different circuit structures achieve. By linking theoretical and experimental studies, we are beginning to reveal the consequences of plasticity mechanisms for network dynamics, in both simple invertebrate circuits and the complex circuits of mammalian cerebral cortex.

Acceleration of Visual System Development by Environmental Enrichment

Abstract: Thus far, the developmental plasticity of the visual system has been studied by altering or reducing visual experience. Here, we investigated whether a complex sensory-motor stimulation, provided by rearing animals in an enriched environment, affects visual system development. We found that raising mice in this condition causes an earlier eye opening, a precocious development of visual acuity, and an accelerated decline of white matter-induced long-term potentiation. These effects are accompanied by a precocious cAMP response element-mediated gene expression and a significant increase of BDNF protein and GAD65/67 expression in enriched pups. In addition, we showed that enriched pups experienced higher levels of licking behavior provided by adult females. Thus, rearing mice from birth in an enriched environment leads to a conspicuous acceleration of visual system development as ascertained at behavioral, electrophysiological, and molecular level.

Clinical disorders of brain plasticity

Abstract: Clinical disorders of brain plasticity are common in the practice of child neurology. Children have an enhanced capacity for brain plasticity compared to adults as demonstrated by their superior ability to learn a second language or their capacity to recover from brain injuries or radical surgery such as hemispherectomy for epilepsy. Basic mechanisms that support plasticity during development include persistence of neurogenesis in some parts of the brain, elimination of neurons through apoptosis or programmed cell death, postnatal proliferation and pruning of synapses, and activity-dependent refinement of neuronal connections. Brain plasticity in children can be divided into four types: adaptive plasticity that enhances skill development or recovery from brain injury; impaired plasticity associated with cognitive impairment; excessive plasticity leading to maladaptive brain circuits; and plasticity that becomes the brain's 'Achilles' Heel' because makes it vulnerable to injury. A broad group of pediatric neurologic disorders can be understood in terms of their impact on fundamental mechanisms for brain plasticity. These include neurofibromatosis, tuberous sclerosis, Fragile X syndrome, other inherited forms of mental retardation, cretinism, Coffin-Lowry syndrome, lead poisoning, Rett syndrome, epilepsy, hypoxic-ischemic encephalopathy and cerebral palsy.

Developmental stress selectively affects the song control nucleus HVC in the zebra finch

Abstract: Songbirds sing complex songs as a result of evolution through sexual selection. The evolution of such sexually selected traits requires genetic control, as well as selection on their expression. Song is controlled by a discrete neural pathway in the brain, and song complexity has been shown to correlate with the volume of specific song control nuclei. As such, the development of these nuclei, in particular the high vocal centre (HVC), is thought to be the mechanism controlling signal expression indicating male quality. We tested the hypothesis that early developmental stress selectively affects adult HVC size, compared with other brain nuclei. We did this by raising cross-fostered zebra finches (Taeniopygia guttata) under stressed and controlled conditions and determining the effect on adult HVC size. Our results confirm the strong influence of environmental conditions, particularly on HVC development, and therefore on the expression of complex songs. The results also show that both environmental and genetic factors affect the development of several brain nuclei, highlighting the developmental plasticity of the songbird brain. In all, these results explain how the complex song repertoires of songbirds can evolve as honest indicators of male quality.

Mitochondria, synaptic plasticity, and schizophrenia.

Abstract: The conceptualization of schizophrenia as a disorder of connectivity, i.e., of neuronal?synaptic plasticity, suggests abnormal synaptic modeling and neuronal signaling, possibly as a consequence of flawed interactions with the environment, as at least a secondary mechanism underlying the pathophysiology of this disorder. Indeed, deficits in episodic memory and malfunction of hippocampal circuitry, as well as anomalies of axonal sprouting and synapse formation, are all suggestive of diminished neuronal plasticity in schizophrenia. Evidence supports a dysfunction of mitochondria in schizophrenia, including mitochondrial hypoplasia, and a dysfunction of the oxidative phosphorylation system, as well as altered mitochondrial-related gene expression. Mitochondrial dysfunction leads to alterations in ATP production and cytoplasmatic calcium concentrations, as well as reactive oxygen species and nitric oxide production. All of the latter processes have been well established as leading to altered synaptic strength or plasticity. Moreover, mitochondria have been shown to play a role in plasticity of neuronal polarity, and studies in the visual cortex show an association between mitochondria and synaptogenesis. Finally, mitochondrial gene upregulation has been observed following synaptic and neuronal activity. This review proposes that mitochondrial dysfunction in schizophrenia could cause, or arise from, anomalies in processes of plasticity in this disorder.

Structural Contributions to Short-Term Synaptic Plasticity

Abstract: Synaptic ultrastructure is critical to many basic hypotheses about synaptic transmission. Various aspects of synaptic ultrastructure have also been implicated in the mechanisms of short-term plasticity. These forms of plasticity can greatly affect synaptic strength during ongoing activity. We review the evidence for how synaptic ultrastructure may contribute to facilitation, depletion, saturation, and desensitization.

A semi-persistent adult ocular dominance plasticity in visual cortex is stabilized by activated CREB.

Abstract: The adult cerebral cortex can adapt to environmental change. Using monocular deprivation as a paradigm, we find that rapid experience-dependent plasticity exists even in the mature primary visual cortex. However, adult cortical plasticity differs from developmental plasticity in two important ways. First, the effect of adult, but not juvenile monocular deprivation is strongly suppressed by administration of barbiturate just prior to recording visual evoked potentials, suggesting that the effect of adult experience can be inactivated acutely. Second, the effect of deprivation is less persistent over time in adults than in juveniles. This correlates with the known decline in CREB function during maturation of the visual cortex. To compensate for this decline in CREB function, we expressed persistently active VP16-CREB and find that it causes adult plasticity to become persistent. These results suggest that in development and adulthood, the regulation of a trans-synaptic signaling pathway controls the adaptive potential of cortical circuits.

Evolutionary biology: adaptive developmental plasticity in snakes.

Abstract: The morphology of organisms is generally well matched to their environment, presumably because expression of their genes is tailored either at the population or the individual level to suit local conditions: for example, snake populations that persistently encounter large prey may accumulate gene mutations that specify a large head size, or head growth may be increased in individual snakes to meet local demands (adaptive developmental plasticity). Here we test the relative contributions of genetics and environment to the jaw sizes of two tiger snake populations: one that consumes small prey on the mainland, and an island population that relies on larger prey and has a larger jaw size. Although the idea of adaptive plasticity in response to environmental pressures is controversial, we find that both factors influence the difference in jaw size between the two populations, and the influence of developmental plasticity is greater in the island population.

Experience-dependent Changes in Basal Dendritic Branching of Layer 2/3 Pyramidal Neurons During a Critical Period for Developmental Plasticity in Rat Barrel Cortex

Abstract: In rat barrel cortex, development of layer 2/3 receptive fields can be disrupted by sensory deprivation, with a critical period ending around postnatal day (PND) 14. To determine if experience-dependent plasticity of dendritic morphology could contribute to the reorganization of synaptic inputs, we analyzed dendritic structure in acute brain slices using two-photon laser scanning microscopy (2PLSM) and automated segmentation and analysis software. Layer 2/3 pyramidal cells from control and deprived rats were imaged from PND 9 to PND 20, spanning the critical period. Detailed analyses were performed on basal arbors, which receive the majority of synaptic input from layer 4. Some parameters (number of primary dendrites, volume subtended, aspect ratios) were stable, suggesting that development of several important properties of basal arbors has ceased by age PND 9. However, the spatial organization of secondary branching changed with age and experience. In older neurons there was a larger fraction of branch points farther from the soma. Deprivation from age PND 9 delayed these changes in secondary branching. This effect of deprivation was rapid (detectable at PND 10) and present at all ages observed. Deprivation initiated at PND 15 had no effect on basal branching measured at PND 20. Thus the spatial organization of secondary dendritic branching is experience-dependent and shares a critical period with receptive field plasticity.

Developmental plasticity of physiology and morphology in diet-restricted European shag nestlings (Phalacrocorax aristotelis).

Abstract: Developmental plasticity of physiology and morphology in diet-restricted European shag nestlings (Phalacrocorax aristotelis)

Synergies between Intrinsic and Synaptic Plasticity in Individual Model Neurons

Abstract: This paper explores the computational consequences of simultaneous intrinsic and synaptic plasticity in individual model neurons. It proposes a new intrinsic plasticity mechanism for a continuous activation model neuron based on low order moments of the neuron's firing rate distribution. The goal of the intrinsic plasticity mechanism is to enforce a sparse distribution of the neuron's activity level. In conjunction with Hebbian learning at the neuron's synapses, the neuron is shown to discover sparse directions in the input.

Modulation of motor function and cortical plasticity in health and disease.

Abstract: Basic science studies demonstrated mechanisms of plasticity and metaplasticity. More recent human studies identified some of these mechanisms as operating in multiple areas of human cognition, such as learning and memory, and in functional recovery from lesions in the CNS, as in stroke. One of the goals of neurorehabilitation is the translation of these principles into rational strategies to promote recovery of function. Understanding the mechanisms and functional role of human plasticity could lead to the development of therapeutic options in situations in which there is virtually no treatment alternative, as in chronic stroke. We review some of the work performed to better understand the substrates and mechanisms underlying cortical plasticity and discuss some experimental approaches to enhance cortical plasticity and recovery of function, like cortical stimulation.

Synaptic and molecular mechanisms regulating plasticity during early learning.

Abstract: Many behaviors are learned most easily during a discrete developmental period, and it is generally agreed that these "sensitive periods" for learning reflect the developmental regulation of molecular or synaptic properties that underlie experience-dependent changes in neural organization and function. Avian song learning provides one example of such temporally restricted learning, and several features of this behavior and its underlying neural circuitry make it a powerful model for studying how early experience sculpts neural and behavioral organization. Here we describe evidence that within the basal ganglia-thalamocortical loop implicated in vocal learning, song acquisition engages N-methyl-d-aspartate receptors (NMDARs), as well as signal transduction cascades strongly implicated in other instances of learning. Furthermore, NMDAR phenotype changes in parallel with developmental and seasonal periods for vocal plasticity. We also review recent studies in the avian song system that challenge the popular notion that sensitive periods for learning reflect developmental changes in the NMDAR that alter thresholds for synaptic plasticity.

Plasticity of the auditory system

Abstract: 1 Overview: Development and Plasticity of the Central Auditory System.- 2 Assembling, Connecting, and Maintaining the Cochlear Nucleus.- 3 Developmental Changes and Cellular Plasticity in the Superior Olivary Complex.- 4 Plasticity of Binaural Systems.- 5 Experience-Dependent Response Plasticity in the Auditory Cortex: Issues, Characteristics, Mechanisms, and Functions.- 6 The Avian Song Control System: A Model for Understanding Changes in Neural Structure and Function.- 7 Plasticity in the Auditory System of Insects.

Experience-dependent neuronal specialization and functional organization in the central auditory area of a songbird.

Abstract: The effect of early experience on brain development was investigated in the central auditory area of a songbird, the field L complex, which is analogous to the mammalian auditory cortex. Multi-unit recordings of auditory responses in the field L complex of adult starlings raised without any experience of adult song during development provide strong evidence of developmental plasticity both in the neuronal responses and in the functional organization of this area. Across the entire area, experimental birds, separated from adults from the age of 1 week old until they were 2 years old, had a much larger number of neurons that responded to all the stimuli than did control birds. The well-known tonotopy demonstrated in adult wild birds using the same procedure was altered. This study is the first to bring evidence of developmental plasticity in the organization of the central auditory areas in songbirds. These results are discussed in relation to other reports on effects of early experience on brain development.

Plasticity and neuroplasticity.

Abstract: (2004). Plasticity and Neuroplasticity. Journal of the History of the Neurosciences: Vol. 13, No. 3, pp. 293-293.

Plasticity of GABAergic synapses in the neonatal rat hippocampus

Abstract: While the development and plasticity of excitatory synaptic connections have been studied into detail, little is known about the development of inhibitory synapses. As proposed for excitatory synapses, recent studies have indicated that activity-dependent forms of synaptic plasticity, such as long-term potentiation and long-term depression, may play a role in the establishment of functional inhibitory synaptic connections. Here, I review these different forms of plasticity and focus on their possible role in the developing neuronal network.

Experience-dependent changes in NMDAR1 expression in the visual cortex of an animal model for amblyopia.

Abstract: When normal binocular visual experience is disrupted during postnatal development, it affects the maturation of cortical circuits and often results in the development of poor visual acuity known as amblyopia. Two main factors contribute to the development of amblyopia: visual deprivation and reduced binocular competition. We investigated the affect of these two amblyogenic factors on the expression of the NMDAR1 subunit in the visual cortex because activation of the NMDA receptor is a key mechanism of developmental neural plasticity. We found that disruption of binocular correlations by monocular deprivation promoted a topographic loss of NMDAR1 expression within the cortical representations of the central visual field and the vertical and horizontal meridians. In contrast, binocular deprivation, which primarily affects visual deprivation, promoted an increase in NMDAR1 expression throughout the visual cortex. These different changes in NMDAR1 expression can be described as topographic and homeostatic plasticity of NMDA expression, respectively. In addition, the changes in NMDA expression in the visual cortex provide a greater understanding of the neural mechanisms that underlie the development of amblyopia and the potential for visual recovery.

Structural plasticity associatedwith exposure to d rugs of abuse

Abstract: Persistent changes in behavior andpsychological function that occur as a function of experience, such those associatedwith learning andmemory, are thought to be d ue to the reorganization of synaptic connections (structural plasticity) in relevant brain circuits Some of the most compelling examples of experience-dependent changes in behavior and psychological function, changes that can last a lifetime, are those that accrue with the development of addictions However, until recently, there has been almost no research on whether potentially addictive drugs produce forms of structural plasticity similar to those associated with other forms of experience-dependent plasticity In this paper we summarize evidence that, indeed, exposure to amphetamine, cocaine, nicotine or morphine produces persistent changes in the structure of dendrites and dendritic spines on cells in brain regions involvedin incentive motivation andreward(such as the nucleus accumbens), andjud gment andthe inhibitory control of behavior (such as the prefrontal cortex) It is suggestedthat structural plasticity associatedwith exposure to d rugs of abuse reflects a reorganization of patterns of synaptic connectivity in these neural systems, a reorganization that alters their operation, thus contributing to some of the persistent sequela associated with drug use—including addiction # 2004 Elsevier Ltd All rights reserved

Parasitism, developmental plasticity and bilateral asymmetry of wing feathers in alpine swift, Apus melba, nestlings

Abstract: The hypothesis that developmental instability is a cost of developmental plasticity is explored using the alpine swift (Apus melba) as a model organism. In a previous study, experimentally parasitized nestlings showed a reduced wing growth rate in the first half of the rearing period when parasites were abundant (i.e. peak infestation) and an accelerated growth rate (i.e. compensatory growth) in the second half when parasites decreased in number. This suggests that alpine swifts are able to adjust growth rate in relation to variation in parasite loads. Because developmental plasticity may entail fitness costs, the energy required to sustain compensatory growth may be invested at the expense of developmental stability, potentially resulting in larger deviations from symmetry in paired, bilateral traits (i.e. fluctuating asymmetry, FA). This hypothesis predicts higher FA in parasitized than deparasitized nestlings because of compensatory growth, and hence individuals sustaining the highest level of compensatory growth rate should exhibit the highest FA levels. Another non-mutually exclusive hypothesis argues that parasites directly cause FA by diverting energy required by host for maintenance and growth, and predicts that individuals suffering the most from parasitism during peak infestation should exhibit the highest FA levels. The present study shows that wing feathers of experimentally parasitized nestlings were more asymmetrical than those of experimentally deparasitized ones 50 days after hatching. Furthermore, in parasitized individuals FA was negatively correlated with wing growth rate during the period of peak infestation but not during the period of compensatory growth. These findings suggest that developmental homeostasis is more sensitive to parasites than to compensatory growth.