Showing papers on "Developmental plasticity published in 2010"
TL;DR: A model whereby the effects of antidepressant treatments could be explained by a reactivation of activity‐dependent and BDNF‐mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges is suggested.
Abstract: Recent evidence suggests that neuronal plasticity plays an important role in the recovery from depression. Antidepressant drugs and electroconvulsive shock treatment increase the expression of several molecules, which are associated with neuronal plasticity, in particular the neurotrophin BDNF and its receptor TrkB. Furthermore, these treatments increase neurogenesis and synaptic numbers in several brain areas. Conversely, depression, at least in its severe form, is associated with reduced volumes of the hippocampus and prefrontal cortex and in at least some cases these neurodegenerative signs can be attenuated by successful treatment. Such observations suggest a central role for neuronal plasticity in depression and the antidepressant effect, and also implicate BDNF signaling as a mediator of this plasticity. The antidepressant fluoxetine can reactivate developmental-like neuronal plasticity in the adult visual cortex, which, under appropriate environmental guidance, leads to the rewiring of a developmentally dysfunctional neural network. These observations suggest that the simple form of the neurotrophic hypothesis of depression, namely, that deficient levels of neurotrophic support underlies mood disorders and increases in these neurotrophic factors to normal levels brings about mood recovery, may not sufficiently explain the complex process of recovery from depression. This review discusses recent data on the role of BDNF and its receptors in depression and the antidepressant response and suggests a model whereby the effects of antidepressant treatments could be explained by a reactivation of activity-dependent and BDNF-mediated cortical plasticity, which in turn leads to the adjustment of neuronal networks to better adapt to environmental challenges.
784 citations
TL;DR: An increase in expression of Lynx1 protein in mice was identified that prevented plasticity in the primary visual cortex late in life, suggesting that modulating the balance between excitatory and inhibitory circuits reactivates visual plasticity and may present a therapeutic target.
Abstract: Experience-dependent brain plasticity typically declines after an early critical period during which circuits are established. Loss of plasticity with closure of the critical period limits improvement of function in adulthood, but the mechanisms that change the brain’s plasticity remain poorly understood. Here, we identified an increase in expression of Lynx1 protein in mice that prevented plasticity in the primary visual cortex late in life. Removal of this molecular brake enhanced nicotinic acetylcholine receptor signaling. Lynx1 expression thus maintains stability of mature cortical networks in the presence of cholinergic innervation. The results suggest that modulating the balance between excitatory and inhibitory circuits reactivates visual plasticity and may present a therapeutic target.
363 citations
TL;DR: How developmental plasticity, although beneficial for short-term survival, can subsequently programme glucose intolerance and insulin resistance in adult life by eliciting changes in key organ structures and the epigenome is highlighted.
Abstract: There are many instances in life when the environment plays a critical role in the health outcomes of an individual, yet none more so than those experienced in fetal and neonatal life. One of the most detrimental environmental problems encountered during this critical growth period are changes in nutrition to the growing fetus and newborn. Disturbances in the supply of nutrients and oxygen to the fetus can not only lead to adverse fetal growth patterns, but they have also been associated with the development of features of metabolic syndrome in adult life. This fetal response has been termed developmental programming or the developmental origins of health and disease. The present review focuses on the epidemiological studies that identified this association and the importance that animal models have played in studying this concept. We also address the potential mechanisms that may underpin the developmental programming of future disease. It also highlights (i) how developmental plasticity, although beneficial for short-term survival, can subsequently programme glucose intolerance and insulin resistance in adult life by eliciting changes in key organ structures and the epigenome, and (ii) how aberrant mitochondrial function can potentially lead to the development of Type 2 diabetes and other features of metabolic syndrome.
311 citations
TL;DR: It is shown that by transplanting embryonic precursors of inhibitory neurons into mice, a period of ocular dominance plasticity can be induced after the end of the normal critical period, suggesting that inhibitory neuron transplantation has therapeutic potential for brain repair and for treating neurological disorders and inducing periods of brain plasticity.
Abstract: Critical periods are times of pronounced brain plasticity. During a critical period in the postnatal development of the visual cortex, the occlusion of one eye triggers a rapid reorganization of neuronal responses, a process known as ocular dominance plasticity. We have shown that the transplantation of inhibitory neurons induces ocular dominance plasticity after the critical period. Transplanted inhibitory neurons receive excitatory synapses, make inhibitory synapses onto host cortical neurons, and promote plasticity when they reach a cellular age equivalent to that of endogenous inhibitory neurons during the normal critical period. These findings suggest that ocular dominance plasticity is regulated by the execution of a maturational program intrinsic to inhibitory neurons. By inducing plasticity, inhibitory neuron transplantation may facilitate brain repair.
265 citations
TL;DR: The results indicate that FMRP is required for the normal developmental progression of synaptic maturation, and loss of this important RNA binding protein impacts the timing of the critical period for layer IV synaptic plasticity.
229 citations
TL;DR: The findings indicate that experience-dependent plasticity of white-matter microstructure extends into old age and that disruptions of structural interhemispheric connectivity in old age, which are pronounced in aging, are modifiable by experience and amenable to treatment.
207 citations
TL;DR: A pragmatic, interdisciplinary definition of neural plasticity is presented that may be used by both clinical and basic scientists studying neurorehabilitation to facilitate the development of novel, more effective rehabilitation interventions.
Abstract: Decades of basic science have clearly demonstrated the capacity of the central nervous system (CNS) to structurally and functionally adapt in response to experience. The field of neurorehabilitation has begun to use this body of work to develop neurobiologically informed therapies that harness the key behavioral and neural signals that drive neural plasticity. The present review describes how neural plasticity supports both learning in the intact CNS and functional improvement in the damaged or diseased CNS. A pragmatic, interdisciplinary definition of neural plasticity is presented that may be used by both clinical and basic scientists studying neurorehabilitation. Furthermore, a description of how neural plasticity may act to drive different neural strategies underlying functional improvement after CNS injury or disease is provided. The understanding of the relationship between these different neural strategies, mechanisms of neural plasticity, and changes in behavior may facilitate the development of novel, more effective rehabilitation interventions.
184 citations
TL;DR: In this formulation, STDP is not itself the basis for explaining other forms of plasticity, but is instead a consequence of changes in the biochemical intermediate, calcium, which act as a more direct trigger of Plasticity mechanisms.
Abstract: Spike timing dependent plasticity (STDP) is a phenomenon in which the precise timing of spikes affects the sign and magnitude of changes in synaptic strength. STDP is often interpreted as the comprehensive learning rule for a synapse - the “first law” of synaptic plasticity. This interpretation is made explicit in theoretical models in which the total plasticity produced by complex spike patterns results from a superposition of the effects of all spike pairs. Although such models are appealing for their simplicity, they can fail dramatically. For example, the measured single-spike learning rule between hippocampal CA3 and CA1 pyramidal neurons does not predict the existence of long-term potentiation. Layers of complexity have been added to the basic STDP model to repair predictive failures, but they have been outstripped by experimental data. We propose an alternate first law: neural activity triggers changes in key biochemical intermediates, which act as a more direct trigger of plasticity mechanisms. One particularly successful model uses intracellular calcium as the intermediate and can account for many observed properties of bidirectional plasticity. In this formulation, STDP is not itself the basis for explaining other forms of plasticity, but is instead a consequence of changes in the biochemical intermediate, calcium. Eventually a mechanism-based framework for learning rules should include other messengers, discrete change at individual synapses, spread of plasticity among neighboring synapses, and priming of hidden processes that change a synapse’s susceptibility to future change. Mechanism-based models provide a rich framework for the computational representation of synaptic plasticity.
171 citations
TL;DR: It is hypothesized that successful cognitive aging requires interactions between these two forms of plasticity, Mechanisms of neural plasticity underpin cognitive plasticity and in turn, neural Plasticity is stimulated by Cognitive plasticity.
Abstract: What is the neurocognitive basis for the considerable individual differences observed in functioning of the adult mind and brain late in life? We review the evidence that in healthy old age the brain remains capable of both neuronal and cognitive plasticity, including in response to environmental and experiential factors. Neuronal plasticity (e.g., neurogenesis, synaptogenesis, cortical re-organization) refers to neuron-level changes that can be stimulated by experience. Cognitive plasticity (e.g., increased dependence on executive function) refers to adaptive changes in patterns of cognition related to brain activity. We hypothesize that successful cognitive aging requires interactions between these two forms of plasticity. Mechanisms of neural plasticity underpin cognitive plasticity and in turn, neural plasticity is stimulated by cognitive plasticity. We examine support for this hypothesis by considering evidence that neural plasticity is stimulated by learning and novelty and enhanced by both dietary manipulations (low-fat, dietary restriction) and aerobic exercise. We also examine evidence that cognitive plasticity is affected by education and training. This is a testable hypothesis which could be assessed in humans in randomized trials comparing separate and combined effects of cognitive training, exercise, and diet on measures of cognitive and brain integrity. Greater understanding of the factors influencing the course of cognitive aging and of the mechanisms underlying those factors could provide information on which people could base choices that improve their ability to age successfully.
163 citations
TL;DR: It is suggested that development and learning are not two completely separate constructs and instead, that they exist on a continuum, which will shed light on behavioral changes across development and, more broadly, about the underlying neural basis of cognition.
Abstract: Development and learning are powerful agents of change across the lifespan that induce robust structural and functional plasticity in neural systems. An unresolved question in developmental cognitive neuroscience is whether development and learning share the same neural mechanisms associated with experience-related neural plasticity. In this article, I outline the conceptual and practical challenges of this question, review insights gleaned from adult studies, and describe recent strides toward examining this topic across development using neuroimaging methods. I suggest that development and learning are not two completely separate constructs and instead, that they exist on a continuum. While progressive and regressive changes are central to both, the behavioral consequences associated with these changes are closely tied to the existing neural architecture of maturity of the system. Eventually, a deeper, more mechanistic understanding of neural plasticity will shed light on behavioral changes across development and, more broadly, about the underlying neural basis of cognition.
127 citations
TL;DR: Convergent evidence is being accumulated for the contention that it is now possible to induce STDP-like changes in the intact human central nervous system by means of TMS to study and interfere with synaptic plasticity in neural circuits in the context of behavior such as learning and memory.
Abstract: Spike-timing dependent plasticity (STDP) has been studied extensively in a variety of animal models during the past decade but whether it can be studied at the systems level of the human cortex has been a matter of debate. Only recently newly developed non-invasive brain stimulation techniques such as transcranial magnetic stimulation (TMS) have made it possible to induce and assess timing dependent plasticity in conscious human subjects. This review will present a critical synopsis of these experiments, which suggest that several of the principal characteristics and molecular mechanisms of TMS-induced plasticity correspond to those of STDP as studied at a cellular level. TMS combined with a second phasic stimulation modality can induce bidirectional long-lasting changes in the excitability of the stimulated cortex, whose polarity depends on the order of the associated stimulus-evoked events within a critical time window of tens of milliseconds. Pharmacological evidence suggests an NMDA receptor mediated form of synaptic plasticity. Studies in human motor cortex demonstrated that motor learning significantly modulates TMS-induced timing dependent plasticity, and, conversely, may be modulated bidirectionally by prior TMS-induced plasticity, providing circumstantial evidence that long-term potentiation-like mechanisms may be involved in motor learning. In summary, convergent evidence is being accumulated for the contention that it is now possible to induce STDP-like changes in the intact human central nervous system by means of TMS to study and interfere with synaptic plasticity in neural circuits in the context of behavior such as learning and memory.
TL;DR: It is argued that invertebrate and vertebrate nervous systems share a common set of mechanisms of synaptic plasticity, and that this situation does not reflect a biological reality and that the opposite is true.
TL;DR: The role of intracortical GABAergic circuitry in controlling both developmental and adult cortical plasticity is examined and its reduction by means of different pharmacological and environmental strategies makes it possible to greatly enhance plasticity in the adult visual cortex, promoting ocular dominance plasticity and recovery from amblyopia.
Abstract: Experience is required for the shaping and refinement of developing neural circuits during well defined periods of early postnatal development called critical periods. Many studies in the visual cortex have shown that intracortical GABAergic circuitry plays a crucial role in defining the time course of the critical period for ocular dominance plasticity. With the end of the critical period, neural plasticity wanes and recovery from the effects of visual defects on visual acuity (amblyopia) or binocularity is much reduced or absent. Recent results pointed out that intracortical inhibition is a fundamental limiting factor for adult cortical plasticity and that its reduction by means of different pharmacological and environmental strategies makes it possible to greatly enhance plasticity in the adult visual cortex, promoting ocular dominance plasticity and recovery from amblyopia. Here we focus on the role of intracortical GABAergic circuitry in controlling both developmental and adult cortical plasticity. We shall also discuss the potential clinical application of these findings to neurological disorders in which synaptic plasticity is compromised because of excessive intracortical inhibition.
TL;DR: Evidence for the role of epigenetic mechanisms in shaping developmental trajectories in response to early life experience as well as the potential plasticity that can occur beyond the perinatal period are discussed.
Abstract: Longitudinal studies in humans demonstrate the association between prenatal and postnatal experiences of adversity and long-term changes in neurodevelopment. These studies raise the question of how experiences become incorporated at a biological level to induce persistent changes in functioning. Laboratory studies using animal models and recent analyses in human cohorts implicate epigenetic mechanisms as a possible route through which these environmental effects are achieved. In particular, there is evidence that changes in DNA methylation are associated with early life experiences with consequences for gene expression and behavior. Despite the potential stability of DNA methylation, it is apparent that this epigenetic mark can be dynamically modified through pharmacological targeting and behavioral experiences. Developmental plasticity may also be achieved through modification of the juvenile environment. Although these juvenile experiences may lead to common endpoints, there is evidence suggesting that the effects of early and later life experiences may be achieved by different molecular pathways. This review discusses evidence for the role of epigenetic mechanisms in shaping developmental trajectories in response to early life experience as well as the potential plasticity that can occur beyond the perinatal period. These studies have implications for approaches to intervention and suggest the importance of considering individual differences in genetic and epigenetic vulnerability in developing treatment strategies.
TL;DR: It is indicated that visual experience induces rapid reorganization of cortical circuitry followed by a period of stabilization, and a close relationship between dynamic changes at single synapses and cortical network function is demonstrated.
Abstract: The impact of activity on neuronal circuitry is complex, involving both functional and structural changes whose interaction is largely unknown. We have used optical imaging of mouse visual cortex responses and two-photon imaging of superficial layer spines on layer 5 neurons to monitor network function and synaptic structural dynamics in the mouse visual cortex in vivo. Total lack of vision due to dark-rearing from birth dampens visual responses and shifts spine dynamics and morphologies toward an immature state. The effects of vision after dark rearing are strongly dependent on the timing of exposure: over a period of days, functional and structural changes are temporally related such that light stabilizes spines while increasing visually driven activity. The effects of long-term light exposure can be partially mimicked by experimentally enhancing inhibitory signaling in the darkness. Brief light exposure, however, results in a rapid, transient, NMDA-dependent increase of cortical responses, accompanied by increased dynamics of dendritic spines. These findings indicate that visual experience induces rapid reorganization of cortical circuitry followed by a period of stabilization, and demonstrate a close relationship between dynamic changes at single synapses and cortical network function.
TL;DR: Recent work has provided insights into the relative contributions of specific astrocytic cues and transporters to synaptic transmission, plasticity, and animal behavior.
TL;DR: This review addresses issues relevant to microRNA function in neurons, in particular, their ability to reinforce developmental decisions and promote synaptic plasticity.
TL;DR: The issue of Treg cell plasticity remains controversial because unequivocal evidence for lineage reprogramming is lacking, and available evidence supports an alternative view of plasticity based on pre-existing heterogeneity of Foxp3(+) T cells as mentioned in this paper.
TL;DR: The induction and expression mechanisms of the induced changes in excitability are described and the functional synergy between synaptic and non-synaptic plasticity and their spatial extent are discussed.
Abstract: Long-lasting plasticity of synaptic transmission is classically thought to be the cellular substrate for information storage in the brain. Recent data indicate however that it is not the whole story and persistent changes in the intrinsic neuronal excitability have been shown to occur in parallel to the induction of long-term synaptic modifications. This form of plasticity depends on the regulation of voltage-gated ion channels. Here we review the experimental evidence for plasticity of neuronal excitability induced at pre- or postsynaptic sites when long-term plasticity of synaptic transmission is induced with Spike-Timing Dependent Plasticity (STDP) protocols. We describe the induction and expression mechanisms of the induced changes in excitability. Finally, the functional synergy between synaptic and non-synaptic plasticity and their spatial extent are discussed.
TL;DR: The data suggest that specific plasticity mechanisms are impaired following early brain injury and that the impairment is associated with altered inhibitory neuronal development and cortical activation.
Abstract: Ocular dominance plasticity (ODP) following monocular deprivation (MD) is a model of activity-dependent neural plasticity that is restricted to an early critical period regulated by maturation of inhibition. Unique developmental plasticity mechanisms may improve outcomes following early brain injury. Our objective was to determine the effects of neonatal cerebral hypoxia-ischemia (HI) on ODP. The rationale extends from observations that neonatal HI results in death of subplate neurons, a transient population known to influence development of inhibition. In rodents subjected to neonatal HI and controls, maps of visual response were derived from optical imaging during the critical period for ODP and changes in the balance of eye-specific response following MD were measured. In controls, MD results in a shift of the ocular dominance index (ODI) from a baseline of 0.15 to -0.10 (p < 0.001). Neonatal HI with moderate cortical injury impairs this shift, ODI = 0.14 (p < 0.01). Plasticity was intact in animals with mild injury and in those exposed to hypoxia alone. Neonatal HI resulted in decreased parvalbumin expression in hemispheres receiving HI compared with hypoxia alone: 23.4 versus 35.0 cells/high-power field (p = 0.01), with no change in other markers of inhibitory or excitatory neurons. Despite abnormal inhibitory neuron phenotype, spontaneous activity of single units and development of orientation selective responses were intact following neonatal HI, while overall visual responses were reduced. Our data suggest that specific plasticity mechanisms are impaired following early brain injury and that the impairment is associated with altered inhibitory neuronal development and cortical activation.
TL;DR: A better understanding of genetic influences on recovery and response to therapy might allow improved treatment after a number of forms of central nervous system injury.
Abstract: Neural plasticity refers to the capability of the brain to alter function or structure in response to a range of events and is a crucial component of both functional recovery after injury and skill learning in healthy individuals. A number of factors influence neural plasticity and recovery of function after brain injury. The current review considers the impact of genetic factors. Polymorphisms in the human genes coding for brain-derived neurotrophic factor and apolipoprotein E have been studied in the context of plasticity and stroke recovery and are discussed here in detail. Several processes involved in plasticity and stroke recovery, such as depression or pharmacotherapy effects, are modulated by other genetic polymorphisms and are also discussed. Finally, new genetic polymorphisms that have not been studied in the context of stroke are proposed as new directions for study. A better understanding of genetic influences on recovery and response to therapy might allow improved treatment after a number of forms of central nervous system injury.
TL;DR: Novel axonal trajectories of layer 2/3 neurons with whisker-related patterns and their developmental plasticity in the mouse somatosensory cortex are uncovered, suggesting that cauterization of whisker follicles results in developmental Plasticity of barrel nets.
Abstract: Elucidating neuronal circuits and their plasticity in the cerebral cortex is one of the important questions in neuroscience research. Here we report novel axonal trajectories and their plasticity in the mouse somatosensory barrel cortex. We selectively visualized layer 2/3 neurons using in utero electroporation and examined the axonal trajectories of layer 2/3 neurons. We found that the axons of layer 2/3 neurons preferentially run in the septal regions of layer 4 and named this axonal pattern "barrel nets." The intensity of green fluorescent protein in the septal regions was markedly higher compared with that in barrel hollows. Focal in utero electroporation revealed that the axons in barrel nets were indeed derived from layer 2/3 neurons in the barrel cortex. During development, barrel nets became visible at postnatal day 10, which was well after the initial appearance of barrels. When whisker follicles were cauterized within 3 d after birth, the whisker-related pattern of barrel nets was altered, suggesting that cauterization of whisker follicles results in developmental plasticity of barrel nets. Our results uncover the novel axonal trajectories of layer 2/3 neurons with whisker-related patterns and their developmental plasticity in the mouse somatosensory cortex. Barrel nets should be useful for investigating the pattern formation and axonal reorganization of intracortical neuronal circuits.
TL;DR: The results indicate that thermal plasticity of wing pattern can be population-specific; thus climate change may lead to a mismatch ofWing pattern to seasonal environment.
Abstract: Temperature is one of the main environmental cues regulating seasonal plasticity in insects. Global climate change may lead to a change in the predictive value of temperature for sea- sonal conditions, potentially resulting in a mismatch of phenotypic form and environment. The afrotropical butterfly Bicyclus anynana shows striking seasonal plasticity for wing patterns and life history traits. This polyphenism is an adaptation to contrasting patterns of rainfall over wet and dry seasons, and is mainly determined by temperature. To investigate the extent of local adaptation of the developmental plasticity response to regional climate, we compared the thermal reaction norms for several life history traits and wing pattern of 2 distant populations from regions with different tem- perature-rainfall associations. We found little to no population differentiation for the life history traits, while wing pattern showed substantially more geographic variation. Broad-sense heritabilities and cross-environment correlations for wing pattern and 2 life history traits indicated a potential for adaptation of the plasticity response of these traits. Our results indicate that thermal plasticity of wing pattern can be population-specific; thus climate change may lead to a mismatch of wing pattern to seasonal environment. Traits that can be further modified by acclimation during the butterfly's adult life span (starvation resistance, resting metabolic rate and egg size) showed no geographic differen- tiation for their developmental plasticity. This indicates that for these traits, adult acclimation plays an important role in coping with local climate.
TL;DR: It is hypothesized that a diversity of phenotypes arranged in developmental sequence throughout an animal's life cycle may have evolved by genetic assimilation of alternative phenotypes originally triggered by environmental cues.
Abstract: Metazoan life cycles can be complex in different ways. A number of diverse phenotypes and reproductive events can sequentially occur along the cycle, and at certain stages a variety of developmenta...
TL;DR: The features of calpains that make them ideally suited to link certain patterns of presynaptic activity to the structural modifications of dendritic spines that could underlie synaptic plasticity and learning and memory are discussed.
Abstract: The family of calcium-dependent neutral proteases, calpains, was discovered more than 30 years ago, but their functional roles in the nervous system under physiological or pathological conditions still remain unclear. Although calpain was proposed to participate in synaptic plasticity and in learning and memory in the early 1980s, the precise mechanism regarding its activation, its target(s) and the functional consequences of its activation have remained controversial. A major issue has been the identification of roles of the two major calpain isoforms present in the brain, calpain-1 and calpain-2, and the calcium requirement for their activation, which exceeds levels that could be reached intracellularly under conditions leading to changes in synaptic efficacy. In this review, we discussed the features of calpains that make them ideally suited to link certain patterns of presynaptic activity to the structural modifications of dendritic spines that could underlie synaptic plasticity and learning and memory. We then summarize recent findings that provide critical answers to the various questions raised by the initial hypothesis, and that further support the idea that, in brain, calpain-2 plays critical roles in developmental and adult synaptic plasticity.
TL;DR: Three independent lines of evidence show that functional inhibition of Bright results in increased developmental plasticity, and suggest that repression of this single molecule confers adult somatic cells with new developmental options.
Abstract: B-cell regulator of immunoglobulin heavy chain transcription (Bright)/ARID3a, an A+T-rich interaction domain protein, was originally discovered in B lymphocyte lineage cells. However, expression patterns and high lethality levels in knockout mice suggested that it had additional functions. Three independent lines of evidence show that functional inhibition of Bright results in increased developmental plasticity. Bright-deficient cells from two mouse models expressed a number of pluripotency-associated gene products, expanded indefinitely, and spontaneously differentiated into cells of multiple lineages. Furthermore, direct knockdown of human Bright resulted in colonies capable of expressing multiple lineage markers. These data suggest that repression of this single molecule confers adult somatic cells with new developmental options.
TL;DR: The goal of this review is to summarize what is known and what is not well understood about developmental changes in functional plasticity at glutamatergic synapses, and in the end, attempt to relate these changes to maturation of neural networks.
Abstract: Overproduction and pruning during develop- ment is a phenomenon that can be observed in the number of organisms in a population, the number of cells in many tissue types, and even the number of synapses on individual neurons. The sculpting of synaptic connections in the brain of a developing organism is guided by its personal experi- ence, which on a neural level translates to specific patterns of activity. Activity-dependent plasticity at glutamatergic synapses is an integral part of neuronal network formation and maturation in developing vertebrate and invertebrate brains. As development of the rodent forebrain transitions away from an over-proliferative state, synaptic plasticity undergoes modification. Late developmental changes in synaptic plasticity signal the establishment of a more stable network and relate to pronounced perceptual and cognitive abilities. In large part, activation of glutamate-sensitive N- methyl-D-aspartate (NMDA) receptors regulates synaptic stabilization during development and is a necessary step in memory formation processes that occur in the forebrain. A developmental change in the subunits that compose NMDA receptors coincides with developmental modifications in synaptic plasticity and cognition, and thus much research in this area focuses on NMDA receptor composition. We pro- pose that there are additional, equally important develop- mental processes that influence synaptic plasticity, includ- ing mechanisms that are upstream (factors that influence NMDA receptors) and downstream (intracellular processes regulated by NMDA receptors) from NMDA receptor acti- vation. The goal of this review is to summarize what is known and what is not well understood about developmen- tal changes in functional plasticity at glutamatergic syn- apses, and in the end, attempt to relate these changes to maturation of neural networks.
TL;DR: It is shown that individuals following alternative developmental pathways in a Swedish population of the butterfly, Pararge aegeria, display differential optimization of adult body mass as a likely response to predictable differences in thermal conditions during reproduction.
Abstract: Switch-induced developmental plasticity, such as the diapause decision in insects, is a major form of adaptation to variable environments. As individuals that follow alternative developmental pathways will experience different selective environments the diapause decision may evolve to a cascade switch that induces additional adaptive developmental differences downstream of the diapause decision. Here, we show that individuals following alternative developmental pathways in a Swedish population of the butterfly, Pararge aegeria, display differential optimization of adult body mass as a likely response to predictable differences in thermal conditions during reproduction. In a more northern population where this type of selection is absent no similar difference in adult mass among pathways was found. We conclude that the diapause decision in the southern population appears to act as a cascade switch, coordinating development downstream of the diapause decision, to produce adult phenotypes adapted to the typical thermal conditions of their expected reproductive period.
TL;DR: Not all neuroplasticity could be explained by activity-dependent models but can be explained if the neural activity involved in the preparatory set directs plasticity, and the temporal and topographic correspondence between Arc and neuro plasticity suggests Arc may be intrinsic to the neuroplasticsity underlying perceptual learning.
Abstract: Models of learning-dependent sensory cortex plasticity require local activity and reinforcement. An alternative proposes that neural activity involved in anticipation of a sensory stimulus, or the preparatory set, can direct plasticity so that changes could occur in regions of sensory cortex lacking activity. To test the necessity of target-induced activity for initial sensory learning, we trained rats to detect a low-frequency sound. After learning, Arc expression and physiologically measured neuroplasticity were strong in a high-frequency auditory cortex region with very weak target-induced activity in control animals. After 14 sessions, Arc and neuroplasticity were aligned with target-induced activity. The temporal and topographic correspondence between Arc and neuroplasticity suggests Arc may be intrinsic to the neuroplasticity underlying perceptual learning. Furthermore, not all neuroplasticity could be explained by activity-dependent models but can be explained if the neural activity involved in the preparatory set directs plasticity.
TL;DR: The noncongruence between treatment and response gradient suggests that different combinations of water velocity have the potential to lead to diverging interpretation of plasticity, both in an ecological and evolutionary context.
Abstract: Developmental plasticity plays a major role in evolution and provides an excellent context for unravelling the ecological implication of variation in abiotic factors to which developing fish are subjected. Water velocity has been known to induce plasticity in salmonids, but the ontogenetic component of these changes is poorly documented. Newly hatched specimens of rainbow trout (Oncorhynchus mykiss) were reared in four constant water velocity treatments (0.4, 0.8, 1.6 and 3.2 cm/sec) for a period of 100 days. Traditional and geometric morphometrics were used complementarily to characterize morphological changes among treatments throughout ontogeny and demonstrated early and complex developmental plasticity in O. mykiss. Certain traits display a constant direction of change, whereas other traits present a break point at 20-25 mm ( approximately 40-60 dph) indicating a modification in the nature of changes between developmental stages. Plasticity in response to water velocity was detected from very early on (15-20 mm; approximately 20-40 dph) and concerned mostly fin-related traits. Body-related traits did not respond conformingly to functional expectations as fishes reared in the fastest velocity treatment show a robust body shape more comparable to that of fish from the slowest treatment than do fish from the intermediate velocity. The noncongruence between treatment and response gradient suggests that different combinations of water velocity have the potential to lead to diverging interpretation of plasticity, both in an ecological and evolutionary context. Overall, the complex shape changes observed in O. mykiss stress the importance of paying better attention to actual functional requirements and adaptations that occur at levels other than hydrodynamics.