Showing papers on "Developmental plasticity published in 2017"
TL;DR: The recent literature is summarized to elaborate the possible mechanistic role of neural plasticity in depression and find findings that may pave the way for future progress in neural Plasticity studies.
Abstract: Neural plasticity, a fundamental mechanism of neuronal adaptation, is disrupted in depression. The changes in neural plasticity induced by stress and other negative stimuli play a significant role in the onset and development of depression. Antidepressant treatments have also been found to exert their antidepressant effects through regulatory effects on neural plasticity. However, the detailed mechanisms of neural plasticity in depression still remain unclear. Therefore, in this review, we summarize the recent literature to elaborate the possible mechanistic role of neural plasticity in depression. Taken together, these findings may pave the way for future progress in neural plasticity studies.
388 citations
TL;DR: It is proposed that critical and sensitive periods of brain development in health and disease can create "windows of opportunity" for neuromodulatory interventions that are not commonly seen in adult brain and probably augment plasticity responses and improve clinical outcomes.
303 citations
TL;DR: Preclinical with clinical work on serotonin and neuroplasticity are linked to bring two pathophysiologic models in clinical depression closer together to enhance clinical treatment of depression.
256 citations
TL;DR: It is suggested that learning and memory rely on an intricate interplay of diverse plasticity mechanisms on different timescales which jointly ensure stability and plasticity of neural circuits.
Abstract: We review a body of theoretical and experimental research on Hebbian and homeostatic plasticity, starting from a puzzling observation: while homeostasis of synapses found in experiments is a slow c...
161 citations
TL;DR: A cross-disciplinary understanding of developmental plasticity is facilitated by highlighting key outstanding questions shared by both evolutionary and health researchers, and by identifying theory and empirical work from both research traditions that is designed to address these questions.
Abstract: Early life experiences can have profound and persistent effects on traits expressed throughout the life course, with consequences for later life behavior, disease risk, and mortality rates. The shaping of later life traits by early life environments, known as 'developmental plasticity', has been well-documented in humans and non-human animals, and has consequently captured the attention of both evolutionary biologists and researchers studying human health. Importantly, the parallel significance of developmental plasticity across multiple fields presents a timely opportunity to build a comprehensive understanding of this phenomenon. We aim to facilitate this goal by highlighting key outstanding questions shared by both evolutionary and health researchers, and by identifying theory and empirical work from both research traditions that is designed to address these questions. Specifically, we focus on: (i) evolutionary explanations for developmental plasticity, (ii) the genetics of developmental plasticity and (iii) the molecular mechanisms that mediate developmental plasticity. In each section, we emphasize the conceptual gains in human health and evolutionary biology that would follow from filling current knowledge gaps using interdisciplinary approaches. We encourage researchers interested in developmental plasticity to evaluate their own work in light of research from diverse fields, with the ultimate goal of establishing a cross-disciplinary understanding of developmental plasticity.
161 citations
TL;DR: This chapter discusses how plasticity is necessary not only for neural networks to acquire new functional properties, but also for them to remain robust and stable.
Abstract: “Neural plasticity” refers to the capacity of the nervous system to modify itself, functionally and structurally, in response to experience and injury. As the various chapters in this volume show, plasticity is a key component of neural development and normal functioning of the nervous system, as well as a response to the changing environment, aging, or pathological insult. This chapter discusses how plasticity is necessary not only for neural networks to acquire new functional properties, but also for them to remain robust and stable. The article also reviews the seminal proposals developed over the years that have driven experiments and strongly influenced concepts of neural plasticity.
138 citations
TL;DR: New insight is gained into the operation and plasticity of CA3 circuits, including the identification of novel forms of synaptic plasticity and their underlying mechanisms, and structural plasticity in the GABAergic control ofCA3 circuits.
Abstract: The CA3 region of the hippocampus is important for rapid encoding of memory. Computational theories have proposed specific roles in hippocampal function and memory for the sparse inputs from the dentate gyrus to CA3 and for the extended local recurrent connectivity that gives rise to the CA3 autoassociative network. Recently, we have gained considerable new insight into the operation and plasticity of CA3 circuits, including the identification of novel forms of synaptic plasticity and their underlying mechanisms, and structural plasticity in the GABAergic control of CA3 circuits. In addition, experimental links between synaptic plasticity of CA3 circuits and memory are starting to emerge.
135 citations
TL;DR: The evidence suggests puberty onset may play a causal role in some aspects of associative neocortical development, but that further research that manipulates puberty and measures gonadal hormones is required.
129 citations
TL;DR: Novel quantal resolution imaging of transmission during locomotive behavior at glutamatergic synapses of the Drosophila larval neuromuscular junction finds that two motor input types, Ib and Is, provide distinct forms of excitatory drive during crawling and differ in key transmission properties.
112 citations
TL;DR: It is proposed that a better understanding of the individual differences that exist within the various mechanisms that govern experience-dependent neuroplasticity will improve the ability to harness brain plasticity for the development of personalized translational strategies for learning and recovery following brain injury or disease.
Abstract: A growing number of research publications have illustrated the remarkable ability of the brain to reorganize itself in response to various sensory experiences. A traditional view of this plastic nature of the brain is that it is predominantly limited to short epochs during early development. Although examples showing that neuroplasticity exists outside of these finite time-windows have existed for some time, it is only recently that we have started to develop a fuller understanding of the different regulators that modulate and underlie plasticity. In this article, we will provide several lines of evidence indicating that mechanisms of neuroplasticity are extremely variable across individuals and throughout the lifetime. This variability is attributable to several factors including inhibitory network function, neuromodulator systems, age, sex, brain disease, and psychological traits. We will also provide evidence of how neuroplasticity can be manipulated in both the healthy and diseased brain, including recent data in both young and aged rats demonstrating how plasticity within auditory cortex can be manipulated pharmacologically and by varying the quality of sensory inputs. We propose that a better understanding of the individual differences that exist within the various mechanisms that govern experience-dependent neuroplasticity will improve our ability to harness brain plasticity for the development of personalized translational strategies for learning and recovery following brain injury or disease.
110 citations
TL;DR: A framework in which impaired synaptic plasticity interacts with brain maturation to yield the emergence of sensory, motor, cognitive, and psychotic features at different times during development in schizophrenia is explored.
TL;DR: This work empirically tested whether personality or behavioural plasticity is responsible for the non-random distribution of shy and bold individuals in a heterogeneous environment and found evidence for bold individuals settling in areas with high human disturbance, but also that birds became bolder with increasing age.
Abstract: An emerging hypothesis of animal personality posits that animals choose the habitat that best fits their personality, and that the match between habitat and personality can facilitate population differentiation, and eventually speciation. However, behavioural plasticity and the adjustment of behaviours to new environments have been a classical explanation for such matching patterns. Using a population of dunnocks (Prunella modularis), we empirically tested whether personality or behavioural plasticity is responsible for the non-random distribution of shy and bold individuals in a heterogeneous environment. We found evidence for bold individuals settling in areas with high human disturbance, but also that birds became bolder with increasing age. Importantly, personality primarily determines the distribution of individuals, and behavioural adjustment over time contributes very little to the observed patterns. We cannot, however, exclude a possibility of very early behavioural plasticity (a type of developmental plasticity) shaping what we refer to as 'personality'. Nonetheless, our findings highlight the role personality plays in shaping population structure, lending support to the theory of personality-mediated speciation. Moreover, personality-matching habitat choice has important implications for population management and conservation.
TL;DR: The expanding sphere of Th17 plasticity is discussed through its shared developmental axes with related cellular subsets such as Th22, Th1, and iTreg in the context of intestinal inflammation and also examines the molecular and epigenetic features of Th 17 cells that mediate these overlapping developmental programs.
Abstract: After emerging from the thymus, naive CD4+ T cells circulate through secondary lymphoid tissues, including gut associated lymphoid tissue of the intestine. The activation of naive CD4 T cells by antigen-presenting cells (APCs) offering cognate antigen initiate differentiation programs that lead to the development of highly specialized T helper (Th) cell lineages. Although initially believed that developmental programing of effector T cells such as T helper 1 (Th1) or T helper 2 (Th2) resulted in irreversible commitment to a fixed fate, subsequent studies have demonstrated greater flexibility, or plasticity, in effector T cell stability than originally conceived. This is particularly so for the Th17 subset, differentiation of which is a highly dynamic process with overlapping developmental axes with inducible regulatory T cells (iTreg), T helper 22 (Th22) and T helper 1 (Th1) cells. Accordingly, intermediary stages of Th17 cells are found in various tissues, which co-express lineage-specific transcription factor(s) or cytokine(s) of developmentally related CD4 T cell subsets. A highly specialized tissue like that of the intestine, which harbors the largest immune compartment of the body, adds several layers of complexity to the intricate process of T helper differentiation. Due to constant exposure to millions of commensal microbes, and periodic exposure to pathogens, the intestinal mucosa maintains a delicate balance between regulatory and effector T cells. It is becoming increasingly clear that equilibrium between tolerogenic and inflammatory axes is maintained in the intestine by shuttling the flexible genetic programming of a developing CD4 T cell along the developmental axis of iTreg, Th17, Th22 and Th1 subsets. Currently, Th17 plasticity remains an unresolved concern in the field of clinical research as targeting Th17 cells to cure immune-mediated disease might also target its related subsets. In this review, we discuss the expanding sphere of Th17 plasticity through its shared developmental axes with related cellular subsets like Th22, Th1, and iTreg in the context of intestinal inflammation and also examine the molecular and epigenetic features of Th17 cells that mediate these overlapping developmental programs.
TL;DR: Using intracellular striatal recordings in intact rats, it is shown that pairing presynaptic and postsynaptic activity induces robust Hebbian bidirectional plasticity, dependent on dopamine and adenosine signaling, which indicates that hebbian corticostriatal plasticity can be induced by classical reinforcement learning mechanisms, and might be central to the acquisition of novel actions.
Abstract: Plasticity at synapses between the cortex and striatum is considered critical for learning novel actions. However, investigations of spike-timing-dependent plasticity (STDP) at these synapses have been performed largely in brain slice preparations, without consideration of physiological reinforcement signals. This has led to conflicting findings, and hampered the ability to relate neural plasticity to behavior. Using intracellular striatal recordings in intact rats, we show here that pairing presynaptic and postsynaptic activity induces robust Hebbian bidirectional plasticity, dependent on dopamine and adenosine signaling. Such plasticity, however, requires the arrival of a reward-conditioned sensory reinforcement signal within 2 s of the STDP pairing, thus revealing a timing-dependent eligibility trace on which reinforcement operates. These observations are validated with both computational modeling and behavioral testing. Our results indicate that Hebbian corticostriatal plasticity can be induced by classical reinforcement learning mechanisms, and might be central to the acquisition of novel actions. Spike timing dependent plasticity (STDP) has been studied extensively in slices but whether such pairings can induce plasticity in vivo is not known. Here the authors report an experimental paradigm that achieves bidirectional corticostriatal STDP in vivo through modulation by behaviourally relevant reinforcement signals, mediated by dopamine and adenosine signaling.
TL;DR: The articles in this issue are focused on different “hot points” in the research area of biochemical mechanisms supporting neuroplasticity.
Abstract: Biochemical processes in synapses and other neuronal compartments underlie neuroplasticity (functional and structural alterations in the brain enabling adaptation to the environment, learning, memory, as well as rehabilitation after brain injury). This basic molecular level of brain plasticity covers numerous specific proteins (enzymes, receptors, structural proteins, etc.) participating in many coordinated and interacting signal and metabolic processes, their modulation forming a molecular basis for brain plasticity. The articles in this issue are focused on different "hot points" in the research area of biochemical mechanisms supporting neuroplasticity.
TL;DR: Depressed patients exhibit a significant interhemispheric difference in motor cortex excitability, an imbalanced inhibitory or excitatory intracortical neurochemical circuitry, reduced postexercise facilitation, and an impaired long-term potentiation-like response to paired-associative transcranial magnetic stimulation, and these symptoms may indicate disrupted plasticity.
Abstract: Neural plasticity is considered the neurophysiological correlate of learning and memory, although several studies have also noted that it plays crucial roles in a number of neurological and psychiatric diseases. Indeed, impaired brain plasticity may be one of the pathophysiological mechanisms that underlies both cognitive decline and major depression. Moreover, a degree of cognitive impairment is frequently observed throughout the clinical spectrum of mood disorders, and the relationship between depression and cognition is often bidirectional. However, most evidence for dysfunctional neural plasticity in depression has been indirect. Transcranial magnetic stimulation has emerged as a noninvasive tool for investigating several parameters of cortical excitability with the aim of exploring the functions of different neurotransmission pathways and for probing in vivo plasticity in both healthy humans and those with pathological conditions. In particular, depressed patients exhibit a significant interhemispher...
TL;DR: It is shown that different OB output layers display unique context-dependent long-term ensemble plasticity, allowing parallel transfer of non-redundant sensory information to downstream centers.
TL;DR: Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostastic plasticity ser...
Abstract: Hebbian and homeostatic plasticity are two major forms of plasticity in the nervous system: Hebbian plasticity provides a synaptic basis for associative learning, whereas homeostatic plasticity ser...
TL;DR: The plasticity evidence indicates that auditory cortex is a component of complex distributed networks that integrate the representation of auditory stimuli with attention, decision and reward processes.
TL;DR: These findings link the O-GlcNAc modification to mammalian neurogenesis and highlight the role of this nutrient-sensing pathway in developmental plasticity and metabolic homeostasis.
TL;DR: The available data suggest that it is complex and well-coordinating nature of these connections that secures optimal synaptic and cellular plasticity in the normal brain.
Abstract: The excitatory neurotransmitter glutamate system and the brain-derived neurotrophic factor (BDNF) system are principally involved in phenomena of cellular and synaptic plasticity. These systems are interacting, and disclosing mechanisms of such interactions is critically important for understanding the machinery of neuroplasticity and its modulation in normal and pathological situations. The short state of evidence in this review addresses experimentally confirmed connections of these mechanisms and their potential relation to the pathogenesis of depression. The connections between the two systems are numerous and bidirectional, providing for mutual regulation of the glutamatergic and BDNF systems. The available data suggest that it is complex and well-coordinating nature of these connections that secures optimal synaptic and cellular plasticity in the normal brain. Both systems are associated with the pathogenesis of depression, and the disturbance of tight and well-balanced associations between them results in unfavorable changes in neuronal plasticity underlying depressive disorders and other mood diseases.
TL;DR: Reconceiving the genotype as an environmental response repertoire rather than a fixed developmental programme leads to three critical evolutionary insights, which suggest a more nuanced understanding of the genotypes and its evolutionary role.
Abstract: In recent decades, the phenotype of an organism (i.e. its traits and behaviour) has been studied as the outcome of a developmental ‘programme’ coded in its genotype. This deterministic view is impl...
TL;DR: The phenotypic plasticity of a broad suite of morphological and life history traits is integrated and shared among species from three geographically independent lineages of mycalesine butterflies, despite considerable periods of independent evolution and exposure to disparate environments.
Abstract: Developmental plasticity is thought to have profound macro-evolutionary effects, for example, by increasing the probability of establishment in new environments and subsequent divergence into independently evolving lineages. In contrast to plasticity optimized for individual traits, phenotypic integration, which enables a concerted response of plastic traits to environmental variability, may affect the rate of local adaptation by constraining independent responses of traits to selection. Using a comparative framework, this study explores the evolution of reaction norms for a variety of life history and morphological traits across five related species of mycalesine butterflies from the Old World tropics. Our data indicate that an integrated response of a suite of key traits is shared amongst these species. Interestingly, the traits that make up the functional suite are all known to be regulated by ecdysteroid signalling in Bicyclus anynana, one of the species included in this study, suggesting the same underlying hormonal regulator may be conserved within this group of polyphenic butterflies. We also detect developmental thresholds for the expression of alternative morphs. The phenotypic plasticity of a broad suite of morphological and life history traits is integrated and shared among species from three geographically independent lineages of mycalesine butterflies, despite considerable periods of independent evolution and exposure to disparate environments. At the same time, we have detected examples of evolutionary change where independent traits show different patterns of reaction norms. We argue that the expression of more robust phenotypes may occur by shifting developmental thresholds beyond the boundaries of the typical environmental variation.
TL;DR: There is increasing evidence that low levels of maternal capital impact the offspring's size at birth, schedule of maturation, and body composition and physiological function in adulthood, and the pathway through which it is attained has major implications for metabolic phenotype.
Abstract: In their seminal book "Worldwide variation in human growth," published in 1976, Eveleth and Tanner highlighted substantial variability within and between populations in the magnitude and schedule of human growth. In the four decades since then, research has clarified why growth variability is so closely associated with human health. First, growth patterns are strongly associated with body composition, both in the short- and long-term. Poor growth in early life constrains the acquisition of lean tissue, while compensatory "catch-up" growth may elevate body fatness. Second, these data are examples of the fundamental link between growth and developmental plasticity. Growth is highly sensitive to ecological stresses and stimuli during early "critical windows," but loses much of this sensitivity as it undergoes canalization during early childhood. Crucially, the primary source of stimuli during early "critical windows" is not the external environment itself, but rather maternal phenotype, which transduces the impact of ecological conditions. Maternal phenotype, representing many dimensions of "capital," thus generates a powerful impact on the developmental trajectory of the offspring. There is increasing evidence that low levels of maternal capital impact the offspring's size at birth, schedule of maturation, and body composition and physiological function in adulthood. While evidence has accrued of substantial heritability in adult height, it is clear that the pathway through which it is attained has major implications for metabolic phenotype. Integrating these perspectives is important for understanding how developmental plasticity may on the one hand contribute to adaptation, while on the other shape susceptibility to non-communicable disease.
TL;DR: The findings show that the effects of developmental plasticity differ between traits, and may be modulated by the different life histories of males and females.
Abstract: Developmental plasticity can match offspring phenotypes to environmental conditions experienced by parents. Such epigenetic modifications are advantageous when parental conditions anticipate offspring environments. Here we show firstly, that developmental plasticity manifests differently in males and females. Secondly, that under stable conditions, phenotypic responses (metabolism and locomotion) accumulate across several generations. Metabolic scope in males was greater at warmer test temperatures (26–36 °C) in offspring bred at warm temperatures (29–30 °C) compared to those bred at cooler temperatures (22–23 °C), lending support to the predictive adaptive hypothesis. However, this transgenerational matching was not established until the second (F2) generation. For other responses, e.g. swimming performance in females, phenotypes of offspring bred in different thermal environments were different in the first (F1) generation, but became more similar across three generations, implying canalization. Thirdly, when environments changed across generations, the grandparental environment affected offspring phenotypes. In females, the mode of the swimming thermal performance curve shifted to coincide with the grandparental rather than the parental or offspring developmental environments, and this lag in response may represent a cost of plasticity. These findings show that the effects of developmental plasticity differ between traits, and may be modulated by the different life histories of males and females.
TL;DR: The data suggest an unanticipated mechanism of developmental compensation whereby cerebellin-1 and neuroligin-3 functionally occlude each other during development of calyx synapses, suggesting developmental plasticity can be a major factor in shaping the overall phenotypes of genetic neuropsychiatric disorders.
Abstract: Neuroligins are postsynaptic cell-adhesion molecules that bind to presynaptic neurexins. Mutations in neuroligin-3 predispose to autism, but how such mutations affect synaptic function remains incompletely understood. Here we systematically examined the effect of three autism-associated mutations, the neuroligin-3 knockout, the R451C knockin, and the R704C knockin, on synaptic transmission in the calyx of Held, a central synapse ideally suited for high-resolution analyses of synaptic transmission. Surprisingly, germline knockout of neuroligin-3 did not alter synaptic transmission, whereas the neuroligin-3 R451C and R704C knockins decreased and increased, respectively, synaptic transmission. These puzzling results prompted us to ask whether neuroligin-3 mutant phenotypes may be reshaped by developmental plasticity. Indeed, conditional knockout of neuroligin-3 during late development produced a marked synaptic phenotype, whereas conditional knockout of neuroligin-3 during early development caused no detectable effect, mimicking the germline knockout. In canvassing potentially redundant candidate genes, we identified developmentally early expression of another synaptic neurexin ligand, cerebellin-1. Strikingly, developmentally early conditional knockout of cerebellin-1 only modestly impaired synaptic transmission, whereas in contrast to the individual single knockouts, developmentally early conditional double knockout of both cerebellin-1 and neuroligin-3 severely decreased synaptic transmission. Our data suggest an unanticipated mechanism of developmental compensation whereby cerebellin-1 and neuroligin-3 functionally occlude each other during development of calyx synapses. Thus, although acute manipulations more likely reveal basic gene functions, developmental plasticity can be a major factor in shaping the overall phenotypes of genetic neuropsychiatric disorders.
TL;DR: Recent discoveries have advanced the understanding of the orchestration of plant developmental switches by transcriptional master regulators, chromatin state changes, and hormone response pathways, with emphasis on the earliest stages of plant development and on the switch from pluripotency to differentiation in different plant organ systems.
Abstract: Plant development is predominantly postembryonic and tuned in to respond to environmental cues. All living plant cells can be triggered to de-differentiate, assume different cell identities, or form a new organism. This developmental plasticity is thought to be an adaptation to the sessile lifestyle of plants. Recent discoveries have advanced our understanding of the orchestration of plant developmental switches by transcriptional master regulators, chromatin state changes, and hormone response pathways. Here, we review these recent advances with emphasis on the earliest stages of plant development and on the switch from pluripotency to differentiation in different plant organ systems.
TL;DR: How plasticity in nonapeptide and steroid actions may influence the expression of, and allow rapid shifts between, sociality and aggression—behavioural shifts that can be particularly important for social interactions are discussed.
Abstract: Endocrine and neuroendocrine systems are key mediators of behavioural plasticity and allow for the ability to shift social behaviour across dynamic contexts. These systems operate across timescales, modulating both rapid responses to environmental changes and developmental plasticity in behavioural phenotypes. Thus, not only do endocrine systems mediate behavioural plasticity, but also the systems themselves exhibit plasticity in functional capabilities. This flexibility at both the mechanistic and behavioural levels can be crucial for reproduction and survival. Here, we discuss how plasticity in nonapeptide and steroid actions may influence the expression of, and allow rapid shifts between, sociality and aggression—behavioural shifts that can be particularly important for social interactions. Recent findings of overlap in the mechanisms that modulate social and aggressive behaviour suggest the potential for a mechanistic continuum between these behaviours. We briefly discuss the potential for a sociality–aggression continuum and novel techniques that will enable probing of the functional connectivity of social behaviours. From an evolutionary perspective, we suggest that plasticity in endocrine and neuroendocrine mechanisms of behaviour may be important targets of selection, and discuss the conditions under which we would predict selection to have resulted in differences in endocrine plasticity across species that differ in social organization. This article is part of the themed issue ‘Physiological determinants of social behaviour in animals’.
TL;DR: A number of studies are reviewed showing that T-type channels participate to numerous homo- and hetero-synaptic plasticity mechanisms that involve different molecular partners and both pre- and post- synapse modifications.
Abstract: The role of T-type calcium currents is rarely considered in the extensive literature covering the mechanisms of long-term synaptic plasticity. This situation reflects the lack of suitable T-type channel antagonists that till recently has hampered investigations of the functional roles of these channels. However, with the development of new pharmacological and genetic tools, a clear involvement of T-type channels in synaptic plasticity is starting to emerge. Here, we review a number of studies showing that T-type channels participate to numerous homo- and hetero-synaptic plasticity mechanisms that involve different molecular partners and both pre- and post-synaptic modifications. The existence of T-channel dependent and independent plasticity at the same synapse strongly suggests a subcellular localization of these channels and their partners that allows specific interactions. Moreover, we illustrate the functional importance of T-channel dependent synaptic plasticity in neocortex and thalamus.