Showing papers on "Developmental plasticity published in 2003"

Phenotypic flexibility and the evolution of organismal design

Abstract: Evolutionary biologists often use phenotypic differences between species and between individuals to gain an understanding of organismal design. The focus of much recent attention has been on developmental plasticity - the environmentally induced variability during development within a single genotype. The phenotypic variation expressed by single reproductively mature organisms throughout their life, traditionally the subject of many physiological studies, has remained under-exploited in evolutionary biology. Phenotypic flexibility, the reversible within-individual variation, is a function of environmental conditions varying predictably (e.g. with season), or of more stochastic fluctuations in the environment. Here, we provide a common framework to bring the different categories of phenotypic plasticity together, and emphasize perspectives on adaptation that reversible types of plasticity might provide. We argue that better recognition and use of the various levels of phenotypic variation will increase the scope for phenotypic experimentation, comparison and integration.

Stress and plasticity in the limbic system.

Abstract: The adult nervous system is not static, but instead can change, can be reshaped by experience Such plasticity has been demonstrated from the most reductive to the most integrated levels, and understanding the bases of this plasticity is a major challenge It is apparent that stress can alter plasticity in the nervous system, particularly in the limbic system This paper reviews that subject, concentrating on: a) the ability of severe and/or prolonged stress to impair hippocampal-dependent explicit learning and the plasticity that underlies it; b) the ability of mild and transient stress to facilitate such plasticity; c) the ability of a range of stressors to enhance implicit fear conditioning, and to enhance the amygdaloid plasticity that underlies it

Bidirectional synaptic plasticity: from theory to reality.

Abstract: Theories of receptive field plasticity and information storage make specific assumptions for how synapses are modified. I give a personal account of how testing the validity of these assumptions eventually led to a detailed understanding of long-term depression and metaplasticity in hippocampal area CA1 and the visual cortex. The knowledge of these molecular mechanisms now promises to reveal when and how sensory experience modifies synapses in the cerebral cortex.

Developmental plasticity of mouse visual acuity.

Abstract: Monocular deprivation in mice between postnatal days 19 and 32 has been reported to significantly shift ocular dominance within the binocular region of primary visual cortex; however, it is not known whether visual deprivation in mice during this physiologically defined critical period also results in amblyopia, as it does in other mammals. We addressed this uncertainty by psychophysically assessing in adulthood (postnatal day 70 or older) the grating acuity of normal and monocularly deprived mice, using the Visual Water Task. The visual acuity of mice tested with their nondeprived eyes was equivalent to that of normal mice ( approximately 0.5 cycles/degree); however, acuity measured with eyes monocularly deprived of vision transiently between postnatal days 19 and 32 was reduced by over 30% ( approximately 0.31 cycles/degree). Identical binocular deprivation produced a significant, but smaller, decrease in acuity ( approximately 0.38 cycles/degree). The effects of monocular and binocular deprivation were long lasting and occurred only if visual deprivation occurred between postnatal days 19 and 32. These data indicate that the deleterious effects of early visual deprivation on visual acuity in mice are similar to those reported in other mammals, and together with electrophysiological evidence of ocular dominance plasticity, suggest that the mechanisms of mouse visual plasticity are fundamentally the same as that in other mammals. Therefore, the mouse is probably a good model for investigating the basic cellular and molecular mechanisms underlying visual developmental plasticity and amblyopia.

Developmental plasticity in respiratory control.

Abstract: Development of the mammalian respiratory control system begins early in gestation and does not achieve mature form until weeks or months after birth. A relatively long gestation and period of postnatal maturation allows for prolonged pre- and postnatal interactions with the environment, including experiences such as episodic or chronic hypoxia, hyperoxia, and drug or toxin exposures. Developmental plasticity occurs when such experiences, during critical periods of maturation, result in long-term alterations in the structure or function of the respiratory control neural network. A critical period is a time window during development devoted to structural and/or functional shaping of the neural systems subserving respiratory control. Experience during the critical period can disrupt and alter developmental trajectory, whereas the same experience before or after has little or no effect. One of the clearest examples to date is blunting of the adult ventilatory response to acute hypoxia challenge by early postnatal hyperoxia exposure in the newborn. Developmental plasticity in neural respiratory control development can occur at multiple sites during formation of brain stem neuronal networks and chemoafferent pathways, at multiple times during development, by multiple mechanisms. Past concepts of respiratory control system maturation as rigidly predetermined by a genetic blueprint have now yielded to a different view in which extremely complex interactions between genes, transcriptional factors, growth factors, and other gene products shape the respiratory control system, and experience plays a key role in guiding normal respiratory control development. Early-life experiences may also lead to maladaptive changes in respiratory control. Pathological conditions as well as normal phenotypic diversity in mature respiratory control may have their roots, at least in part, in developmental plasticity.

Homeostatic plasticity in the CNS: synaptic and intrinsic forms

Abstract: The study of experience-dependent plasticity has been dominated by questions of how Hebbian plasticity mechanisms act during learning and development. This is unsurprising as Hebbian plasticity constitutes the most fully developed and influential model of how information is stored in neural circuits and how neural circuitry can develop without extensive genetic instructions. Yet Hebbian plasticity may not be sufficient for understanding either learning or development: the dramatic changes in synapse number and strength that can be produced by this kind of plasticity tend to threaten the stability of neural circuits. Recent work has suggested that, in addition to Hebbian plasticity, homeostatic regulatory mechanisms are active in a variety of preparations. These mechanisms alter both the synaptic connections between neurons and the intrinsic electrical properties of individual neurons, in such a way as to maintain some constancy in neuronal properties despite the changes wrought by Hebbian mechanisms. Here we review the evidence for homeostatic plasticity in the central nervous system, with special emphasis on results from cortical preparations.

Eye opening induces a rapid dendritic localization of PSD-95 in central visual neurons

Abstract: The membrane-associated guanylate kinase PSD-95 scaffolds N-methyl-d-aspartate receptors to cytoplasmic signaling molecules, and associates with other glutamate receptors at central synapses. However, regulation of PSD-95 in vivo is poorly understood. We provide evidence of an activity-dependent redistribution of PSD-95 to dendrites in central visual neurons that is tied to eye opening. Six hours after eye opening, increased dendritic PSD-95 coimmunoprecipitates with the same proportions of stargazin, increased proportions of the N-methyl-d-aspartate receptor subunit NR2A, and decreased proportions of NR2B. Sustained high levels of PSD-95 in dendrites are dependent on continued pattern vision in juvenile but not mature animals, suggesting that the stabilization of PSD-95 at synapses may be involved in the control of developmental plasticity.

Decline of the critical period of visual plasticity is concurrent with the reduction of NR2B subunit of the synaptic NMDA receptor in layer 4.

Abstract: The specific composition of NMDA receptor subunits is thought to underlie the developmental plasticity of the cortex revealed by unbalanced binocular stimulation. However, evidence that NR2 subunits change in correlation with the critical period at locations that are relevant to visual plasticity has been missing. Using preembedding and postembedding immunostaining, as well as electron microscopy, we quantified the volumetric densities of NR1-, NR2A-, and NR2B-containing synapses in layers 4 and 2/3 of the ferret visual cortex at different postnatal ages. Before eye opening, NR2A is encountered infrequently at postsynaptic sites in layer 4, but it increases sharply by postnatal day 34. In the subsequent weeks, postsynaptic NR2A labeling increases gradually in both layers 4 and 2/3 to become the most prevalent subunit in the adult animal. The NR2B subunit is the more prevalent subunit at the onset of the critical period of cortical plasticity. However, it displays different developmental patterns in layers 4 and 2/3. Although no change occurs in synaptic NR2B density in layer 2/3, in layer 4, NR2B maintains its high levels through the peak of the critical period and then becomes significantly reduced by the end of the peak of the critical period. This low level is maintained throughout adulthood. Our results demonstrate a correlation between the loss of NR2B subunits from layer 4 synaptic sites and the decline of the critical period, suggesting that the presence of NR2B subunits at synaptic sites could be a permissive factor regulating the ocular dominance plasticity of the developing cortex.

Cooler butterflies lay larger eggs: developmental plasticity versus acclimation

Abstract: We use a full factorial design to investigate the effects of maternal and paternal developmental temperature, as well as female oviposition temperature, on egg size in the butterfly Bicyclus anynana. Butterflies were raised at two different temperatures and mated in four possible sex-by-parental-temperature crosses. The mated females were randomly divided between high and low oviposition temperatures. On the first day after assigning the females to different temperatures, only female developmental temperature affected egg size. Females reared at the lower temperature laid larger eggs than those reared at a higher temperature. When eggs were measured again after an acclimation period of 10 days, egg size was principally determined by the prevailing temperature during oviposition, with females ovipositing at a lower temperature laying larger eggs. In contrast to widely used assumptions, the effects of developmental temperature were largely reversible. Male developmental temperature did not affect egg size in either of the measurements. Overall, developmental plasticity and acclimation in the adult stage resulted in very similar patterns of egg size plasticity. Consequently, we argue that the most important question when testing the significance of acclamatory changes is not at which stage a given plasticity is induced, but rather whether plastic responses to environmental change are adaptive or merely physiological constraints.

Comment on "Little evidence for developmental plasticity of adult hematopoietic stem cells".

Abstract: Wagers et al . ([1][1]) investigated the possibility of marrow cell plasticity at the single cell level, as we did ([2][2]). Although they found “little evidence for developmental plasticity”— i.e., marrow cells giving rise to mesoderm (blood), endoderm (liver), and ectoderm (brain)—their

Sexual dimorphism in gender plasticity and its consequences for breeding system evolution

Abstract: Flowering plants are able to develop gametes throughout their lives. As a consequence, environmental conditions can impact this development and alter a plant's functional gender or the degree to which it achieves fitness through male or female function. Two dimorphic breeding systems are widespread among angiosperm families: gynodioecy (hermaphrodites and females) and dioecy (males and females). Gynodioecy can evolve into dioecy, via loss of female function on the hermaphrodites, or it can remain stable. Here I discuss how developmental plasticity of gender can impact the sex ratio of populations and thereby influence the transition of one breeding system into another. I review studies showing that greater plasticity of fruit production by hermaphrodites as compared with females causes sex ratios among populations to vary in response to environmental conditions, with higher female frequency expected in harsh or low-quality sites. I also review how dioecy may evolve in dry sites to avoid inbreeding and any consequent inbreeding depression. Taken together, these studies show the importance of understanding how ecological development affects functional gender and consequently the evolutionary stability or malleability of dimorphic breeding systems.

Mutations in deadly seven/notch1a Reveal Developmental Plasticity in the Escape Response Circuit

Abstract: The relatively simple neural circuit driving the escape response in zebrafish offers an excellent opportunity to study properties of neural circuit formation. The hindbrain Mauthner cell is an essential component of this circuit. Mutations in the zebrafish deadly seven/notch1a (des) gene result in supernumerary Mauthner cells. We addressed whether and how these extra cells are incorporated into the escape-response circuit. Calcium imaging revealed that all Mauthner cells in desb420 mutants were active during an elicited escape response. However, the kinematic performance of the escape response in mutant larvae was very similar to wild-type fish. Analysis of the relationship between Mauthner axon collaterals and spinal neurons revealed that there was a decrease in the number of axon collaterals per Mauthner axon in mutant larvae compared with wild-type larvae, indicative of a decrease in the number of synapses formed with target spinal neurons. Moreover, we show that Mauthner axons projecting on the same side of the nervous system have primarily nonoverlapping collaterals. These data support the hypothesis that excess Mauthner cells are incorporated into the escape-response circuit, but they divide their target territory to maintain a normal response, thus demonstrating plasticity in the formation of the escape-response circuit. Such plasticity may be key to the evolution of the startle responses in mammals, which use larger populations of neurons in circuits similar to those in the fish escape response.

Rearing in different photic and spectral environments changes the optomotor response to chromatic stimuli in the cichlid fish Aequidens pulcher

Abstract: Developmental plasticity of spectral processing in vertebrates was investigated in fish by using an innate behavior, the optomotor response. Rearing blue acara (Aequidens pulcher; Cichlidae) under white lights of different intensities as well as deprivation of long wavelengths induced significant changes in the animals' responses to chromatic stimuli. Deprivation of short wavelengths had no effect. With this and previous studies on animals reared under similar conditions, we have demonstrated that developmental plasticity in spectral processing is present at a wide range of neural levels, spanning from photoreceptors to behavior. We hypothesize that earlier studies did not reveal such effects because of the rearing and testing conditions used.

Experience-dependent plasticity for auditory processing in a raptor.

Abstract: A growing consensus in the neurosciences is that neural plasticity remains open throughout life, often driven by critical experiences ([1][1]). Almost all of the work on plasticity in vertebrates comes from studies in captivity using restrained animals and neurophysiological preparations; most are

A synthetic peptide ligand of NCAM affects exploratory behavior and memory in rodents

Abstract: The neural cell adhesion molecule (NCAM) is an important modulator of neuronal development and plasticity associated with learning and memory. Previously, a synthetic peptide ligand of NCAM, called C3, has been identified and shown to modulate neuronal plasticity in vitro and memory in a step-through passive avoidance task in rats in vivo. In this study, we extended these findings and found that intraventricular injection of C3 prior to training impaired learning or memory processes in rats and mice in an approach avoidance task and decreased exploratory behavior in rats. The effect of C3 was additionally evaluated in the Morris water maze; memory impairment was observed in the second training trial 24 h after the injection of C3 only, indicating an effect on short-term memory. The C3-mediated memory impairment observed in the approach avoidance and water maze tests is suggested to be the result of C3-inhibiting NCAM functions in the brain. This study demonstrates that it is possible to modulate learning/memory processes in rodents in vivo with small synthetic NCAM-binding peptides that induce developmental plasticity in vitro.

Reciprocal Interaction of Sleep and Synaptic Plasticity

Abstract: Synaptic plasticity underlying learning and memory has been proposed, on the basis of several experimental approaches, to be intimately related with sleep: 1) The idea that sleep contributes to stabilization of acquired memory arises from numerous studies depriving subjects or animals of sleep. 2) Evidence from developing technologies supports "offline" reprocessing of recent experiences during sleep. 3) Recent analysis of the thalamocortical system establishes the reciprocal observation that sleep itself is a plastic process affected by waking experience. This overview synthesizes these converging perspectives across a variety of brain regions and species. We propose the developing visual pathway as a fruitful model for comprehensive understanding of sleep and synaptic plasticity.

Plasticity in the Human Nervous System: The nature and mechanisms of plasticity

Abstract: It is nowwell established that the functional organization of the cerebral cortex isplastic, that is, changes inorganizationoccur throughout life in response to normal as well as abnormal experience. The potential for reorganization hasbeendemonstrated inboth sensoryandmotor areasof adult cortex, either as a consequence of trauma, pathological changes, manipulation of sensory experience, or learning. These changes can only be evaluated with reference to an extensive experimental base that has identified a repeatable representation pattern (e.g. somatotopy, tonotopy, or retinotopy), for which change can be detected.While the scope of changes are often at the edge of our technical capabilities to assess, there are striking examples of significant and rapid change (for reviews, see SanesD Buonomano&Merzenich, 1998). There is an overwhelming belief that modifications in cortical organization emerge through changes in synaptic efficacy within the cortex and elsewhere in the nervous system. Further, these changes are have been closely linked to the phenomena called long-termpotentiation (LTP) and long-term depression (LTD). This review deals mainly with the changes that have been detected in themotor cortex and their link to synapticmodification. Some of the most convincing evidence that learning and practice influences cortical organization and that learning operates through LTP/D-mediated mechanisms has come through work in the motor cortex. This work is also of profound significance to the medical community because it implies that the impaired or damagedmotor cortex can be restructured through appropriate physical rehabilitation schemes or through pharmacologicalmeans that alter mechanisms accounting for LTP/D.

Spike-driven synaptic plasticity for learning correlated patterns of mean firing rates.

Abstract: Long term synaptic changes induced by neural spike activity are believed to underlie learning and memory. Spike-driven long-term synaptic plasticity has been investigated in simplified situations in which the patterns of mean rates to be encoded were statistically independent. An additional regulatory mechanism is required to extend the learning capability to more complex and natural stimuli. This mechanism can be provided by those effects of the action potentials that are believed to be responsible for spike-timing dependent plasticity. These effects, when combined with the dependence of synaptic plasticity on the post-synaptic depolarization, produce the non-monotonic learning rule needed for storing correlated patterns of mean rates.

Homeostasis and Learning through Spike-Timing Dependent Plasticity

Abstract: Synaptic plasticity is thought to be the neuronal correlate of learning. Moreover, modification of synapses contributes to the activity-dependent homeostatic maintenance of neurons and neural networks. In this chapter, we review theories of synaptic plasticity and show that both homeostatic control of activity and detection of correlations in the presynaptic input can arise from spike-timing dependent plasticity (STDP). Relations to classical rate-based Hebbian learning are discussed.

IGF-1 induces neonatal climbing-fibre plasticity in the mature rat cerebellum.

Abstract: Following unilateral transection (pedunculotomy) of the neonatal rat olivocerebellar pathway, the remaining inferior olive reinnervates the denervated hemicerebellum with correct topography. The critical period for this transcommissural reinnervation closes between postnatal days 7 and 10 but can be extended by injection of growth factors. Whether growth factor treatment can extend developmental plasticity into a mature, myelinated milieu remains unknown. Rats aged 11-30 days, underwent unilateral pedunculotomy followed 24 h later by injection of insulin-like growth factor 1 (IGF-1) into the denervated cerebellum. In all animals, IGF-1 induced transcommissural olivocerebellar reinnervation, which displayed organisation consistent with normal olivocerebellar topography even following pedunculotomy up to day 20. Thus IGF-1 can reproduce developmental neuroplasticity to promote appropriate target reinnervation in a mature myelinated environment.

Plasticity in respiratory motor control

Abstract: Neural plasticity reflects a long-lasting functional change based on prior experience and is certainly important in a wide range of adaptive responses. Remarkable progress has been made in understanding the basis of neuroplasticity, especially in an attempt to decipher the mechanisms underlying

Rehabilitation of Attention

Abstract: In this paper, evidence is reviewed for separable attention systems in the brain, and it is argued a) that attention may have a privileged role in mediating experience dependent plasticity in the brain and b) that at least some types of attention may be capable of rehabilitation following brain damage.

Stimulation-induced plasticity in the human motor cortex

Abstract: Introduction Neuronal plasticity may be defined as any functional change within the nervous system outlasting an (experimental) manipulation Plasticity, by this definition, does not comprise structural changes, such as those occurring during development or repair Although there is no universally accepted lower limit of its duration, the term ‘plasticity’ is usually only applied when neuronal changes outlast the manipulation by more than a few seconds In experimental animals, as well as in humans, plasticity is usually defined neurophysiologically by changes in the stimulus–response characteristics (‘excitability’) Plasticity of the central nervous system has attracted much interest because it is thought to be related to the mechanisms underlying the formation of memories and the learning of new skills Very likely, it is also involved in restoration of brain function after its initial loss as a consequence of brain injury Neuronal plasticity may be induced internally, such as by practising movements (see Chapter 4), or externally, for instance, by limb amputation, spinal cord injury or cerebral stroke (see Chapter 8), or by repetitive electrical or magnetic neuronal stimulation, as reviewed here Models of plasticity relying on external stimulation may be attractive because they allow best to control for experimental conditions Human models of central nervous system plasticity may contribute particularly relevant information to the understanding of fundamental principles of plasticity Additionally, the neuronal changes induced in human models of plasticity may themselves prove to be therapeutically useful

Altered neuronal responses to feeding-relevant peptides as sign of developmental plasticity in the hypothalamic regulatory system of body weight.

Abstract: Neuronal plasticity during the critical postnatal period of development seems to promote a change in the function of the hypothalamic regulatory system of body weight. Rats raised in small litters (SL) of only three pups per mother compared to ten or twelve in control litters (CL) gain significantly more weight than normal rats till weaning and are overweight also in later life. These rats are known to express hyperleptinemia, hyperglycemia and hyperinsulinemia. The review summarizes the results of action of leptin and insulin as well as of several feeding-relevant neuropeptides on neuronal activity of hypothalamic regulatory centres in overweight SL rats compared to controls. The study was performed on brain slices perfused with solution containing 10 mM glucose. Whereas a normally inhibitory action of leptin and insulin on medial arcuate neurons (ArcM) is reduced in SL rats and partly replaced by activation, the normally activating effect of these hormones on ventromedial (VMH) neurons is altered to predominant inhibition. Inhibition of ArcM neurons may decrease the release of the orexigenic neuropeptide Y (NPY) and agouti gene-related protein (AGRP). Thus, the negative feedback by leptin and insulin on food intake is replaced by diminished response and partly positive feedback processes in SL rats. The action of NPY and AGRP as well as of the orexigenic melanin-concentrating hormone on paraventricular (PVH) and VMH neurons is also shaped from activation or bimodal effects to predominant inhibition. Such inhibition of PVH and VMH might lead to reduced energy expenditure in small litter rats. Also the anorexigenic melanocortin alpha-MSH seems to contribute into increased energy storage. These altered responses of hypothalamic neurons in overweight small litter rats might reflect a general mechanism of neurochemical plasticity and "malprogramming" of hypothalamic neuropeptidergic systems leading to a permanently altered regulatory function.