Showing papers on "Developmental plasticity published in 2007"
TL;DR: This study systematically characterized synaptic plasticity of retrovirally labeled adult-born dentate granule cells at different stages during their neuronal maturation, demonstrating that adult- born neurons exhibit the same classic critical period plasticity as neurons in the developing nervous system.
904 citations
TL;DR: It is proposed that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course, allowing genotypic variation to be preserved through transient environmental changes.
Abstract: Biomedical science has little considered the relevance of life history theory and evolutionary and ecological developmental biology to clinical medicine. However, the observations that early life influences can alter later disease risk--the "developmental origins of health and disease" (DOHaD) paradigm--have led to a recognition that these perspectives can inform our understanding of human biology. We propose that the DOHaD phenomenon can be considered as a subset of the broader processes of developmental plasticity by which organisms adapt to their environment during their life course. Such adaptive processes allow genotypic variation to be preserved through transient environmental changes. Cues for plasticity operate particularly during early development; they may affect a single organ or system, but generally they induce integrated adjustments in the mature phenotype, a process underpinned by epigenetic mechanisms and influenced by prediction of the mature environment. In mammals, an adverse intrauterine environment results in an integrated suite of responses, suggesting the involvement of a few key regulatory genes, that resets the developmental trajectory in expectation of poor postnatal conditions. Mismatch between the anticipated and the actual mature environment exposes the organism to risk of adverse consequences-the greater the mismatch, the greater the risk. For humans, prediction is inaccurate for many individuals because of changes in the postnatal environment toward energy-dense nutrition and low energy expenditure, contributing to the epidemic of chronic noncommunicable disease. This view of human disease from the perspectives of life history biology and evolutionary theory offers new approaches to prevention, diagnosis and intervention.
869 citations
TL;DR: 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 and these associations are thought to be consequences of developmental plasticity.
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. Coronary heart disease and the disorders related to it arise through a series of interactions between environmental influences and the pathways of development that preceded them. These diseases are the product of branching pathways of development in which the branchings are triggered by the environment before and after birth.
674 citations
TL;DR: There is now considerable evidence that elements of the heritable or familial component of disease susceptibility are transmitted by nongenomic means, and that environmental influences acting during early development shape disease risk in later life.
Abstract: There is now considerable evidence that elements of the heritable or familial component of disease susceptibility are transmitted by nongenomic means, and that environmental influences acting during early development shape disease risk in later life. The underlying mechanisms are thought to involve epigenetic modifications in nonimprinted genes induced by aspects of the developmental environment, which modify gene expression without altering DNA sequences. These changes result in life-long alterations in gene expression. Such nongenomic tuning of phenotype through developmental plasticity has adaptive value because it attempts to match an individual's responses to the environment predicted to be experienced. When the responses are mismatched, disease risk increases. An example of such mismatch is that arising either from inaccurate nutritional cues from the mother or placenta before birth, or from rapid environmental change through improved socioeconomic conditions, which contribute substantially to the increasing prevalence of type-2 diabetes, obesity, and cardiovascular disease. Recent evidence suggests that the effects can be transmitted to more than the immediately succeeding generation, through female and perhaps male lines. Future research into epigenetic processes may permit us to develop intervention strategies.
520 citations
TL;DR: This work used two-photon calcium imaging to investigate whether homeostatic response regulation contributes to changes of eye-specific responsiveness after monocular deprivation in mouse visual cortex and found that deprived-eye responses were either weaker or stronger after MD, depending on the amount of open-eye input a cell received.
348 citations
TL;DR: It is reported that the effects of neonatal leptin on hepatic gene expression and epigenetic status in adulthood are directionally dependent on the animal's nutritional status in utero, suggesting the potential for a discontinuous distribution of environmentally induced phenotypes, analogous to the phenomenon of polyphenism.
Abstract: Developmental plasticity in response to environmental cues can take the form of polyphenism, as for the discrete morphs of some insects, or of an apparently continuous spectrum of phenotype, as for most mammalian traits. The metabolic phenotype of adult rats, including the propensity to obesity, hyperinsulinemia, and hyperphagia, shows plasticity in response to prenatal nutrition and to neonatal administration of the adipokine leptin. Here, we report that the effects of neonatal leptin on hepatic gene expression and epigenetic status in adulthood are directionally dependent on the animal's nutritional status in utero. These results demonstrate that, during mammalian development, the direction of the response to one cue can be determined by previous exposure to another, suggesting the potential for a discontinuous distribution of environmentally induced phenotypes, analogous to the phenomenon of polyphenism.
308 citations
TL;DR: This article argues that the thrifty phenotype is the consequence of three different adaptive processes ‐ niche construction, maternal effects, and developmental plasticity ‐ all of which in humans are influenced by the authors' large brains.
Abstract: Human diseases in adulthood are increasingly associated with growth patterns in early life, implicating early-life nutrition as the underlying mechanism. The thrifty phenotype hypothesis proposed that early-life metabolic adaptations promote survival, with the developing organism responding to cues of environmental quality by selecting an appropriate trajectory of growth. Recently, some authors have proposed that the thrifty phenotype is also adaptive in the longer-term, by preparing the organism for its likely adult environment. However, windows of plasticity close early during human development, and subsequent environmental changes may result in the selected trajectory becoming inappropriate, leading to adverse effects on health. This paradox generates uncertainty as to whether the thrifty phenotype is indeed adaptive for the offspring in humans. The thrifty phenotype should not be considered a dichotomous concept, rather it refers to the capacity of all offspring to respond to environmental information during early ontogenetic development. This article argues that the thrifty phenotype is the consequence of three different adaptive processes - niche construction, maternal effects, and developmental plasticity - all of which in humans are influenced by our large brains. While developmental plasticity represents an adaptation by the offspring, both niche construction and parental effects are subject to selection on parental rather than offspring fitness. The three processes also operate at different paces. Human offspring do not become net calories-producers until around 18 years of age, such that the high energy costs of the human brain are paid primarily by the mother, even after weaning. The evolutionary expansion of human brain volume occurred in environments characterised by high volatility, inducing strong selective pressure on maternal capacity to provision multiple offspring simultaneously. The thrifty phenotype is therefore best considered as a manipulation of offspring phenotype for the benefit of maternal fitness. The information that enters offspring phenotype during early development does not predict the likely future environment of the offspring, but rather reflects the mother’s own developmental experience and the quality of the environment during her own maturation. Offspring growth trajectory thus becomes aligned with long-term maternal capacity to provision. In contemporary populations, the sensitivity of offspring development to maternal phenotype exposes the offspring to adverse effects, through four distinct pathways. The offspring may be exposed to (1) poor maternal metabolic control (e.g. gestational diabetes), (2) maternally derived toxins (e.g. maternal smoking), or (3) low maternal social status (e.g. small size). Adverse consequences of these effects may then be exacerbated by (4) exposure either to the “toxic” western environment in postnatal life, in which diet and physical activity levels are mismatched with metabolic experience in utero, or at the other extreme to famine. The rapid emergence of the epidemic of the metabolic syndrome in the 20th Century reflects the rapid acceleration in the pace of niche construction relative to the slower physiological combination of developmental plasticity and parental effects.
262 citations
TL;DR: Recent exciting findings in the field of experience-dependent plasticity are discussed that advance the understanding of mechanisms underlying the activation, expression, and closure of critical periods in the visual system.
211 citations
TL;DR: Experimental results that demonstrate experience-dependent plasticity in the central auditory representations of sound frequency, level and temporal sequence, as well as in the representations of binaural localization cues in both developing and adult animals are reviewed.
185 citations
TL;DR: The conceptual basis of the 'developmental origins' paradigm has converged on the role of developmental plasticity responding to signals from the early environment, with heightened risk of disease if the induced phenotype does not match the later environment.
Abstract: The conceptual basis of the 'developmental origins' paradigm has converged on the role of developmental plasticity responding to signals from the early environment, with heightened risk of disease if the induced phenotype does not match the later environment. Nevertheless, numerous questions remain, including the current burden of disease that can be attributed to early environmental factors; the pathways, mechanisms and windows of plasticity; the identification of early markers of environmentally induced change; and the feasibility, costs and benefits of intervention. A focused agenda of research is needed to convince policy makers of the importance of developmental factors in human disease.
169 citations
TL;DR: Efficient therapeutic interventions in the injured CNS should combine targeted manipulations of growth control mechanisms with task-specific training and rehabilitation paradigms to maintain specific patterns of connectivity in the highly complex mammalian CNS.
TL;DR: The connection between environmental heterogeneity and developmental plasticity at the island population level is demonstrated, and the importance of the interplay between local specialization and phenotypic plasticity depending on the local selection pressures is highlighted.
Abstract: Although theoretical models have identified environmental heterogeneity as a prerequisite for the evolution of adaptive plasticity, this relationship has not yet been demonstrated experimentally. Because of pool desiccation risk, adaptation of development rate is important for many amphibians. In a simulated pool-drying experiment, we compared the development time and phenotypic plasticity in development time of populations of the common frog Rana temporaria, originating from 14 neighbouring islands off the coast of northern Sweden. Drying regime of pools used by frogs for breeding differed within and among the islands. We found that the degree of phenotypic plasticity in development time was positively correlated with the spatial variation in the pool-drying regimes present on each island. In addition, local adaptation in development time to the mean drying rate of the pools on each island was found. Hence, our study demonstrates the connection between environmental heterogeneity and developmental plasticity at the island population level, and also highlights the importance of the interplay between local specialization and phenotypic plasticity depending on the local selection pressures.
TL;DR: By controlling spike timing and sculpting neuronal rhythms, inhibitory interneurons play a key role in regulating neuronal circuits and behavior in the regulation of sleep, anxiety, memory, sensorimotor processing and post‐natal developmental plasticity.
Abstract: By controlling spike timing and sculpting neuronal rhythms, inhibitory interneurons play a key role in regulating neuronal circuits and behavior. The pronounced diversity of GABAergic (gamma-aminobutyric acid) interneurons is paralleled by an extensive diversity of GABAA receptor subtypes. The region- and domain-specific location of these receptor subtypes offers the opportunity to gain functional insights into the role of defined neuronal circuits. These developments are reviewed with regard to the regulation of sleep, anxiety, memory, sensorimotor processing and post-natal developmental plasticity.
TL;DR: A series of experiments demonstrates that global histone acetylation, induced by HDAC inhibition, can partially reverse the lineage restriction of OPCs, thereby inducing developmental plasticity.
Abstract: Recently, it was demonstrated that lineage-committed oligodendrocyte precursor cells (OPCs) can be converted to multipotent neural stem-like cells, capable of generating both neurons and glia after exposure to bone morphogenetic proteins. In an effort to understand and control the developmental plasticity of OPCs, we developed a high-throughput screen to identify novel chemical inducers of OPC reprogramming. Using this system, we discovered that inhibition of histone deacetylase (HDAC) activity in OPCs acts as a priming event in the induction of developmental plasticity, thereby expanding the differentiation potential to include the neuronal lineage. This conversion was found to be mediated, in part, through reactivation of sox2 and was highly reproducible at the clonal level. Further, genome-wide expression analysis demonstrated that HDAC inhibitor treatment activated sox2 and 12 other genes that identify or maintain the neural stem cell state while simultaneously silencing a large group of oligodendrocyte lineage-specific genes. This series of experiments demonstrates that global histone acetylation, induced by HDAC inhibition, can partially reverse the lineage restriction of OPCs, thereby inducing developmental plasticity.
TL;DR: It is demonstrated that taking a developmental perspective is extremely valuable for understanding the ecology of inducible defenses and the ability of snails to completely reverse their defenses was limited to early in ontogeny due to the constraints associated with modular growth of shell material.
Abstract: Inducible defenses allow prey to modulate their phenotypic responses to the level of predation risk in the environment and reduce the cost of constitutive defenses. Inherent in this statement is that prey must alter their phenotypes during development in order to form these defenses. This has lead many ecologists and evolutionary biologists to call for studies that examine developmental plasticity to provide insights into the importance of development in controlling the trajectories of trait formation, the integration of phenotypes over ontogeny, and the establishment of developmental windows for trait formation and reversal. By moving away from studies that focus on a single point in development, we can obtain a more complete understanding of the phenotypic decisions and limitations of prey. We exposed freshwater snails (Helisoma trivolvis) to environments in which predatory water bugs (Belostoma flumineum) were always absent, always present, or added and removed at different points in development. We discovered that snails formed morphological defenses against water bugs. Importantly, after the initial induction of defenses, snails showed similar developmental trajectories as snails reared without predators. Further, the snails possessed wide developmental windows for inducible defenses that extended past sexual maturity. However, being induced later in development appeared to have an associated cost (i.e., decreased shell thickness) that was not found when water bugs were always present. This epiphenotype (i.e., new shell formation as an extension of the current shell) suggests that resource limitation plays an important role in responses to temporal variation in predation risk and may have critical ecological costs that limit the benefits of the inducible defense. Lastly, the ability of snails to completely reverse their defenses was limited to early in ontogeny due to the constraints associated with modular growth of shell material. In sum, we demonstrate that taking a developmental perspective is extremely valuable for understanding the ecology of inducible defenses.
TL;DR: Emerging evidence that mitochondria play important roles in regulating developmental and adult neuroplasticity is reviewed, suggesting a therapeutic potential for approaches that target mitochondrial mechanisms.
Abstract: The structure and function of neurons is dynamic during development and in adaptive responses of the adult nervous system to environmental demands. The mechanisms that regulate neuronal plasticity are poorly understood, but are believed to involve neurotransmitter and neurotrophic factor signaling pathways. In the present article, I review emerging evidence that mitochondria play important roles in regulating developmental and adult neuroplasticity. In neurons, mitochondria are located in axons, dendrites, growth cones and pre- and post-synaptic terminals where their movements and functions are regulated by local signals such as neurotrophic factors and calcium influx. Mitochondria play important roles in fundamental developmental processes including the establishment of axonal polarity and the regulation of neurite outgrowth, and are also involved in synaptic plasticity in the mature nervous system. Abnormalities in mitochondria are associated with neurodegenerative and psychiatric disorders, suggesting a therapeutic potential for approaches that target mitochondrial mechanisms.
TL;DR: There is evidence that the nonclassical auditory pathways in adults may be activated through expression of neural plasticity, causing cross-modal interaction in some individuals with tinnitus.
Abstract: There is considerable evidence that expression of neural plasticity plays a central role in the development of the abnormalities that cause many forms of tinnitus. Expression of neural plasticity can change the balance between excitation and inhibition, promote hyperactivity, and cause re-organization of specific parts of the nervous system or redirection of information to parts of the nervous system not normally involved in processing of sounds (such as the non-classical, or extralemniscal pathways). The strongest promoter of expression of neural plasticity is deprivation of input, which explains why tinnitus often occurs together with hearing loss or injury to the auditory nerve.
TL;DR: It is argued that a critical component of current and future research on adaptive plasticity in the skull, and especially cranial joints, should employ a multifaceted characterization of a functional system, one that incorporates data on myriad tissues so as to evaluate the role of altered load versus differential tissue response on the anatomical, cellular and molecular processes that contribute to the strength of such composite structures.
Abstract: Excessive, repetitive and altered loading have been implicated in the initiation of a series of soft- and hard-tissue responses or ;functional adaptations' of masticatory and locomotor elements. Such adaptive plasticity in tissue types appears designed to maintain a sufficient safety factor, and thus the integrity of given element or system, for a predominant loading environment(s). Employing a mammalian species for which considerable in vivo data on masticatory behaviors are available, genetically similar domestic white rabbits were raised on diets of different mechanical properties so as to develop an experimental model of joint function in a normal range of physiological loads. These integrative experiments are used to unravel the dynamic inter-relationships among mechanical loading, tissue adaptive plasticity, norms of reaction and performance in two cranial joint systems: the mandibular symphysis and temporomandibular joint (TMJ). Here, we argue that a critical component of current and future research on adaptive plasticity in the skull, and especially cranial joints, should employ a multifaceted characterization of a functional system, one that incorporates data on myriad tissues so as to evaluate the role of altered load versus differential tissue response on the anatomical, cellular and molecular processes that contribute to the strength of such composite structures. Our study also suggests that the short-term duration of earlier analyses of cranial joint tissues may offer a limited notion of the complex process of developmental plasticity, especially as it relates to the effects of long-term variation in mechanical loads, when a joint is increasingly characterized by adaptive and degradative changes in tissue structure and composition. Indeed, it is likely that a component of the adaptive increases in rabbit TMJ and symphyseal proportions and biomineralization represent a compensatory mechanism to cartilage degradation that serves to maintain the overall functional integrity of each joint system. Therefore, while variation in cranial joint anatomy and performance among sister taxa is, in part, an epiphenomenon of interspecific differences in diet-induced masticatory stresses characterizing the individual ontogenies of the members of a species, this behavioral signal may be increasingly mitigated in over-loaded and perhaps older organisms by the interplay between adaptive and degradative tissue responses.
TL;DR: Interestingly, recent work from the lab indicates that the enhanced synaptic localization of NMDA receptors promotes increases in the size of dendritic spines, which may represent a structural-based mechanism that supports the formation and stabilization of maladapted synaptic connections that, in a sense, "fix" the addictive behavior in the adolescent and young adult brain.
Abstract: It is now known that brain development continues into adolescence and early adulthood and is highly influenced by experience-dependent adaptive plasticity during this time. Behaviorally, this period is also characterized by increased novelty seeking and risk-taking. This heightened plasticity appears to be important in shaping behaviors and cognitive processes that contribute to proper development of an adult phenotype. However, increasing evidence has linked these same experience-dependent learning mechanisms with processes that underlie drug addiction. As such, the adolescent brain appears to be particularly susceptible to experience-dependent learning processes associated with consumption of alcohol and addictive drugs. At the level of the synapse, homeostatic changes during ethanol consumption are invoked to counter the destabilizing effects of ethanol on neural networks. This homeostatic response may be especially pronounced in the adolescent and young adult brain due to its heightened capacity to undergo experience-dependent changes, and appears to involve increased synaptic targeting of NMDA receptors. Interestingly, recent work from our lab also indicates that the enhanced synaptic localization of NMDA receptors promotes increases in the size of dendritic spines. This increase may represent a structural-based mechanism that supports the formation and stabilization of maladapted synaptic connections that, in a sense, "fix" the addictive behavior in the adolescent and young adult brain.
TL;DR: It is suggested that heterochronic shifts in ossification can not only buffer development under fluctuating environments while maintaining epigenetic sensitivity critical for normal skeletal formation, but also enable epigenetically induced gene expression to generate specialized morphological adaptations.
Abstract: Evolutionary diversifications are commonly attributed to the continued modifications of a conserved genetic toolkit of developmental pathways, such that complexity and convergence in organismal forms are assumed to be due to similarity in genetic mechanisms or environmental conditions. This approach, however, confounds the causes of organismal development with the causes of organismal differences and, as such, has only limited utility for addressing the cause of evolutionary change. Molecular mechanisms that are closely involved in both developmental response to environmental signals and major evolutionary innovations and diversifications are uniquely suited to bridge this gap by connecting explicitly the causes of within-generation variation with the causes of divergence of taxa. Developmental pathways of bone formation and a common role for bone morphogenetic proteins (BMPs) in both epigenetic bone remodeling and the evolution of major adaptive diversifications provide such opportunity. We show that variation in timing of ossification can result in similar phenotypic patterns through epigenetically induced changes in gene expression and propose that both genetic accommodation of environmentally induced developmental pathways and flexibility in development across environments evolve through heterochronic shifts in bone maturation relative to exposure to unpredictable environments. We suggest that such heterochronic shifts in ossification can not only buffer development under fluctuating environments while maintaining epigenetic sensitivity critical for normal skeletal formation, but also enable epigenetically induced gene expression to generate specialized morphological adaptations. We review studies of environmental sensitivity of BMP pathways and their regulation of formation, remodeling, and repair of cartilage and bone to examine the hypothesis that BMP-mediated skeletal adaptations are facilitated by evolved reactivity of BMPs to external signals. Surprisingly, no empirical study to date has identified the molecular mechanism behind developmental plasticity in skeletal traits. We outline a conceptual framework for future studies that focus on mediation of phenotypic plasticity in skeletal development by the patterns of BMP expression.
TL;DR: This work examines the bases of the developmental plasticity in a model species, B. anynana, and also the evolution of key adult life history traits, including starvation resistance and longevity, and now understands something about the processes that generate variation in the phenotype, and about the ecological context of responses to environmental stress.
Abstract: Plasticity is a crucial component of the life cycle of invertebrates that live as active adults throughout wet and dry seasons in the tropics. Such plasticity is seen in the numerous species of Bicyclus butterfl ies in Africa which exhibit seasonal polyphenism with sequential generations of adults with one or other of two alternative phenotypes. These differ not only in wing pattern but in many other traits. This divergence across a broad complex of traits is associated with survival and reproduction either in a wet season that is favourable in terms of resources, or mainly in a dry season that is more stressful. This phenomenon has led us to examine the bases of the developmental plasticity in a model species, B. anynana, and also the evolution of key adult life history traits, including starvation resistance and longevity. We now understand something about the processes that generate variation in the phenotype, and also about the ecological context of responses to environmental stress. The responses clearly involve a mix of developmental plasticity as cued by different environments in pre-adult development, and the acclimation of life history traits in adults to their prevailing environment.
TL;DR: This work shows that short-term synaptic plasticity endows models of cortical circuits with a remarkable stability in the low-activity regime and the contribution of synaptic dynamics to this stability can be predicted on the basis of general principles from control theory.
Abstract: Numerous experimental data show that cortical networks of neurons are not silent in the absence of external inputs, but rather maintain a low spontaneous firing activity. This aspect of cortical networks is likely to be important for their computational function, but is hard to reproduce in models of cortical circuits of neurons because the low-activity regime is inherently unstable. Here we show-through theoretical analysis and extensive computer simulations-that short-term synaptic plasticity endows models of cortical circuits with a remarkable stability in the low-activity regime. This short-term plasticity works as a homeostatic mechanism that stabilizes the overall activity level in spite of drastic changes in external inputs and internal circuit properties, while preserving reliable transient responses to signals. The contribution of synaptic dynamics to this stability can be predicted on the basis of general principles from control theory.
TL;DR: From these new studies, two roles emerge for Cdk5 in plasticity: one in which it controls structural plasticity via phosphorylation of synaptic substrates, and a second where it regulates functional plasticity through protein‐protein interactions.
Abstract: Protein kinases mediate the intracellular signal transduction pathways controlling synaptic plasticity in the central nervous system. While the majority of protein kinases achieve this function via the phosphorylation of synaptic substrates, some kinases may contribute through alternative mechanisms in addition to enzymatic activity. There is growing evidence that protein kinases may often play structural roles in plasticity as well. Cyclin-dependent kinase 5 (Cdk5) has been implicated in learning and synaptic plasticity. Initial scrutiny focused on its enzymatic activity using pharmacological inhibitors and genetic modifications of Cdk5 cofactors. Quite recently Cdk5 has been shown to govern learning and plasticity via regulation of glutamate receptor degradation, a function that may not dependent on phosphorylation of downstream effectors. From these new studies, two roles emerge for Cdk5 in plasticity: one in which it controls structural plasticity via phosphorylation of synaptic substrates, and a second where it regulates functional plasticity via protein-protein interactions.
TL;DR: The developmental plasticity that accounts for the ill health of humans who are living in conditions of rapid economic change is commonplace in biology and understanding the evolutionary background sets the developmental origins of ill health in humans in context and has profound implications for public health.
Abstract: Fetal experience determines some of the characteristics of human adults. Well-nourished mothers have offspring who are adapted to affluent conditions; mothers on a low level of nutrition have offspring who are adapted to lean environments. If the mother's forecast of her offspring's future environment is incorrect, the health of her offspring may suffer severely. The developmental plasticity that accounts for the ill health of humans who are living in conditions of rapid economic change is commonplace in biology. Understanding the evolutionary background sets the developmental origins of ill health in humans in context and has profound implications for public health.
TL;DR: It is suggested that developmental responses of traits plasticity and interaction at critical ontogenetic periods are congruent with specific environmental conditions to maintain the functional integrity of the organism.
Abstract: Environmental conditions such as temperature and water velocity may induce changes among alternative developmental pathways, i.e. phenotypic responses, in vertebrates. However, the extent to which the environment induces developmental plasticity and integrated developmental responses during early ontogeny of fishes remains poorly documented. We analyzed the responses of newly hatched Arctic charr (Salvelinus alpinus) to four experimental water velocities during 100 days of development. To our knowledge, this work is the first to analyze developmental plasticity responses of body morphology to an experimental gradient of water velocities during early ontogeny of fish. Arctic charr body size and shape responses show first, that morphometric traits display significant differences between low and high water velocities, thus revealing directional changes in body traits. Secondly, trait variation allows the recognition of critical ontogenetic periods that are most responsive to environmental constraints (40-70 and 80-90 days) and exhibit different levels of developmental plasticity. This is supported by the observation of asynchronous timing of variation peaks among treatments. Third, morphological interaction of traits is developmentally plastic and time-dependent. We suggest that developmental responses of traits plasticity and interaction at critical ontogenetic periods are congruent with specific environmental conditions to maintain the functional integrity of the organism.
TL;DR: Investigating effects of parental, developmental and acclimation temperature on life-history traits in the butterfly Bicyclus anynana finds between-generation temperature effects on larval time, pupal time, larval growth rate and egg size were qualitatively very similar to effects of developmental temperature, and additionally affected pupal mass but not egg number.
01 Jan 2007
TL;DR: This book discusses the search for memory in the brain, the Brain Lesion Approach and the Dynamic Nature of Learning and Memory Systems, and the Brain Neurochemical Cascades Underlie Modification of Neural Circuits.
TL;DR: It is concluded that early after stroke, use-dependent plasticity is impaired in the perinfarct cortex.
Abstract: Spontaneous restorative plasticity is reported frequently after stroke To test whether conditions in perinfarct cortex facilitate plastic changes, we examined experience-dependent plasticity of cortical functional representation of vibrissae in rat brain after focal photothrombotic stroke Cortical activation was visualized with [C]2-deoxyglucose To induce plasticity, four rows of whiskers were trimmed on one side of the snout for a month, whereas one row was spared This deprivation was started immediately after the stroke In control rats, cortical representation of the spared row whiskers was significantly enlarged compared with undeprived controls In rats with infarct posterior to the barrel cortex, no plastic change of the spared row representation was observed We conclude that early after stroke, use-dependent plasticity is impaired in the perinfarct cortex
TL;DR: Results from the application of electrical and magnetic stimulation of the auditory and the somatosensory cortices are used for treatment of tinnitus and for alleviating some forms of pain in support of the Darwinian hypothesis about neural plasticity.
Abstract: We present the hypothesis that expression of neural plasticity is a form of adaptation based on natural selection, where cells or cell groups deprived of sensory input actively go and look for information in order to survive. The Darwinian model of brain plasticity can explain the symptomatology induced by deprivation of input which was not well explained by classical plasticity without contradicting pertinent data from the neurophysiological, neuroanatomical, functional neuroimaging, and clinical literature. Applying the concept of Darwinian plasticity to sensory plasticity that causes symptoms and signs of disease might lead to the development of new treatments for deprivation of input induced symptomatology. We will use results from the application of electrical and magnetic stimulation of the auditory and the somatosensory cortices for treatment of tinnitus and for alleviating some forms of pain in support of the Darwinian hypothesis about neural plasticity. We will also review the literature regarding physiological and anatomical, as well as imaging data that support the existence of this hypothetical form of plasticity.