Showing papers on "Developmental plasticity published in 1999"

Silent synapses in neural plasticity: current evidence.

Abstract: Silent synapses, defined as structural specializations for neurotransmission that do not produce a physiological response in the receiving cell, may occur frequently in neural circuits. Their recruitment to physiological effectiveness may be an important component of circuit modification. In several nervous systems, evidence from electrophysiological and optophysiological measurements has established a strong case for the existence of silent synapses and for their emergence as active synapses with appropriate stimulation. During normal development and aging, synapses of individual neurons change in number, and many of these may be functionally silent at certain stages of their developmental trajectory. Changes in their status may contribute to shaping the properties of neural pathways during development, often in response to neural activity. In general, it is often difficult to distinguish physiological emergence of pre-established silent synapses from developmental maturation or de novo formation of new synapses. Several possible mechanisms for silent synapses and their recruitment are reviewed. These include incompletely assembled synapses that lack structural components, insufficient availability of key presynaptic proteins, and nonfunctional postsynaptic receptors, or presence of receptors that do not mediate a postsynaptic response except under specific conditions (conditionally silent synapses). The available silent synapses can often be rapidly activated, and conversely, active synapses appear to be rapidly silenced in many instances. These properties enable silent synapses to participate in short-term facilitation and depression. In addition, they may contribute to long-term facilitation and potentiation, especially during development.

Steroid-induced developmental plasticity in hypothalamic astrocytes: implications for synaptic patterning.

Abstract: We have previously demonstrated that astrocytes in the developing arcuate nucleus of the rat hypothalamus exhibit a sexually dimorphic morphology as a result of differential exposure to gonadal steroids. Testosterone via its aromatized byproduct, estrogen, induces arcuate astrocytes to undergo differentiation during the first few days of life. These differentiated astrocytes exhibit a stellate morphology. Coincident with the steroid-induced increase in astrocyte differentiation is a reduction of dendritic spines on arcuate neurons. As a result, the arcuate nucleus of males has fewer axodendritic spine synapses than females and this dimorphism is retained throughout life. In the immediately adjacent ventromedial nucleus, neonatal astrocytes are immature and unresponsive to steroids. Neurons in this region show no change in dendritic spines in the first few days of life but do exhibit increased dendritic branching as a result of testosterone exposure. These findings illustrate the importance of distinct populations of astrocytes in restricted brain regions and their potential importance to the establishment of regionally specific synaptic patterning. Conflicting reports leave the site of steroid-mediated astrocyte responsiveness in the arcuate nucleus unresolved: Are gonadal steroids acting directly on astrocytes or are steroid-concentrating neurons mediating astrocytic responsiveness? In this review, we discuss the current understanding of astrocyte-neuron interactions and the possible mechanisms for steroid-mediated, astrocyte-directed synaptic patterning in the developing hypothalamus.

Insulin-like growth factors as mediators of functional plasticity in the adult brain.

Abstract: Insulin-like growth factors (IGFs) are present in the brain throughout life. While their role as modulators of brain growth and differentiation during development is becoming apparent, their possible involvement in adult brain function is less known. Nevertheless, accumulating evidence indicates a role for IGFs in brain plasticity processes. Specifically, IGFs modulate synaptic efficacy by regulating synapse formation, neurotransmitter release and neuronal excitability. IGFs also provide constant trophic support to target cells in the brain and in this way maintain appropriate neuronal function. Pathological dearrangement of this trophic input may lead to brain disease. Molecular targets of the IGFs in the adult brain may include pre- and post-synaptic proteins involved in synaptic contacts, membrane channels, neurite-guiding molecules, extracellular matrix components and glial-derived intercellular messengers. Future studies on the role of IGFs in the adult brain may help unravel the relationship between neuronal plasticity and brain disease.

Mechanisms of experience-dependent plasticity in the auditory localization pathway of the barn owl.

Abstract: Sound localization is a computational process that requires the central nervous system to measure various auditory cues and then associate particular cue values with appropriate locations in space. Behavioral experiments show that barn owls learn to associate values of cues with locations in space based on experience. The capacity for experience-driven changes in sound localization behavior is particularly great during a sensitive period that lasts until the approach of adulthood. Neurophysiological techniques have been used to determine underlying sites of plasticity in the auditory space-processing pathway. The external nucleus of the inferior colliculus (ICX), where a map of auditory space is synthesized, is a major site of plasticity. Experience during the sensitive period can cause large-scale, adaptive changes in the tuning of ICX neurons for sound localization cues. Large-scale physiological changes are accompanied by anatomical remodeling of afferent axons to the ICX. Changes in the tuning of ICX neurons for cue values involve two stages: (1) the instructed acquisition of neuronal responses to novel cue values and (2) the elimination of responses to inappropriate cue values. Newly acquired neuronal responses depend differentially on NMDA receptor currents for their expression. A model is presented that can account for this adaptive plasticity in terms of plausible cellular mechanisms.

From visual experience to visual function: roles of neurotrophins.

Abstract: Recently, a role for neurotrophins in regulating cortical developmental plasticity has clearly emerged. We present in this review a summary of the early data on the action of nerve growth factor (NGF) in visual cortical development and plasticity in the rat and of other neurotrophins in the visual cortex of other mammals. In addition, to clarify the differences in the results obtained with the various neurotrophins in different animal preparations, we also report new data on the action of NGF, brain-derived neurotrophic factor (BDNF), neurotrophin (NT)3, and NT4 in the same preparation-namely, the visual cortex of the rat. We discuss old and new results in a physiological model in which different neurotrophins play different roles in regulating visual cortical development and plasticity by acting on different neural targets, such as lateral geniculate nucleus (LGN) afferents, intracortical circuitry, and subcortical afferents, and propose a tentative scheme summarizing these actions.

Impaired Experience-dependent Plasticity in Barrel Cortex of Mice Lacking the Alpha and Delta Isoforms of CREB

Abstract: The transcription factor cyclic-AMP response element binding protein (CREB) has been implicated in long-term plasticity processes in vertebrate and invertebrate species. In the absence of the alpha/delta CREB isoforms, performance is impaired in long-term memory tasks and the long-term maintenance of long-term potentiation (LTP) is impaired in the hippocampus. However, it is not known whether CREB plays a role in neocortical plasticity. Antibodies to CREB revealed that CREB-immunoreactive nuclei are present in all cortical layers but are more numerous in layers II/III, where they composed at least two-thirds the total population of cells. CREB-immunopositive cells were therefore present and densest in the very cortical layers that exhibit experience-dependent plasticity at this age. In order to assess the role of CREB in neocortical plasticity, we studied the effect of vibrissae deprivation on receptive field plasticity in the barrel cortex of mutant mice lacking the alpha/delta isoforms of CREB. A single vibrissa was spared and the others removed for 18 days. In wild-types this caused potentiation of the spared vibrissa response. However, in adult mutants (>6 months) spared vibrissa responses from homozygotes were potentiated less than in any adolescent animals or in adult wild-type littermates. Surround receptive field responses were abnormally large in homozygotes and failed to increase by the same amount as they did in wild-types. In contrast, the alpha/delta CREB mutation had no discernible effect on plasticity in cortical layers II/III of the younger adolescent age group (1-2 months), suggesting that different plasticity processes may operate at this age. Further tests showed that the beta isoform of CREB was up-regulated in the barrel cortex of the alpha/delta CREB knock-outs, suggesting that this subunit may have compensated partly for the loss of the alpha/delta isoforms. These studies suggests that CREB plays a role in experience-dependent plasticity in the adult neocortex.

Molecular analysis of developmental plasticity in neocortex.

Abstract: Gene expression studies indicate that during activity-dependent developmental plasticity, N-methyl-D-aspartate receptor activation causes a Ca(2+)-dependent increase in expression of transcription factors and their downstream targets. The products of these plasticity genes then operate collectively to bring about the structural and functional changes that underlie ocular dominance plasticity in visual cortex. Identifying and characterizing plasticity genes provides a tool for molecular dissection of the mechanisms involved. Members of second-messenger pathways identified in adult plasticity paradigms and elements of the transmission machinery are the first candidate plasticity genes tested for their role in activity-dependent developmental plasticity. Knockout mice with deletions of such genes have allowed analyzing their function in the context of different systems and in different paradigms. Studies of mutant mice reveal that activity-dependent plasticity is not necessarily a unified phenomenon. The relative importance of a gene can vary with the context of its expression during different forms of plasticity. Forward genetic screens provide additional new candidates for testing, some with well-defined cellular functions that provide insight into possible plasticity mechanisms.

Neuronal plasticity : building a bridge from the laboratory of the clinic

Abstract: Pathological Mutations of Nicotinic Receptors and Nicotine-Based Therapies for Brain Disorders.- Towards an Ecology of Cortical Organisation: Experience and the Changing Brain.- Pain and Neuroplasticity.- Auditory Cortical Plasticity and Sensory Substitution.- Functional Relevance of Cortical Plasticity.- "Anomalous" Representations and Perceptions: Implications for Human Neuroplasticity.- Neuroplasticity in the Adjustment to Blindness.- The Perception of Actions: Its Putative Effect on Neural Plasticity.- Evidence for Four Forms of Neuroplasticity.- Imaging Investigations of Human Brain Plasticity.- Connectionist Modeling of Relearning and Generalization in Acquired Dyslexic Patients.- Some Neurological Principles Relevant to the Origins of - and the Cortical Plasticity-Based Remediation of - Developmental Language Impairments.

Cortical plasticity in normal and abnormal cognitive development: evidence and working hypotheses.

Abstract: In this paper I review evidence and viewpoints on developmental plasticity in the cerebral cortex. Although there is some degree of plasticity in the cortex during early postnatal life in the human infant, this plasticity is constrained by various factors. Three working hypotheses about postnatal cortical specialization of function are advanced, and some specific predictions about the limits and extent of plasticity are assessed through both empirical evidence from infants and simulations on simple cortical network models.

Theoretical aspects of neuroplasticity.

Abstract: The authors propose an integrative theory of the organization of neuroplastic processes. Neuroplasticity is assumed to be one of the essential characteristics of the nervous tissue which may be manifested comparatively rapidly and result in reversible changes (functional plasticity). It may also modulate the expression of genotype into phenotype (adaptation) and thus bring about long-lasting effects. Neuroplastic mechanisms are triggered by various natural or artificial stimuli, which may arise in the internal or external environment, and they may differ quantitatively or qualitatively. The effects of plasticity can lead to either positive or negative changes during development (evolutionary plasticity), after short-term exposition (reactive plasticity), after long-term or continuous stimuli (adaptational plasticity), and during functional or structural recovery of damaged neuronal circuits (reparation plasticity). Manifestations of plasticity have probably the same basis, irrespective of the cause which triggered them or the brain region where they were accomplished. Neuroplastic mechanisms are based on the modulation of signal transmission across synapses. They can be related to interneuronal relations. The resulting changes may occur in the communication between neurons (synaptic level), in the activity of local neuronal circuits (at the level of local circuits) or in the relations between individual functional brain systems (multimodular level).

Neuromodulation, development and synaptic plasticity.

Abstract: We discuss parallels in the mechanisms underlying use-dependent synaptic plasticity during development and long-term potentiation (LTP) and long-term depression (LTD) in neocortical synapses. Neuromodulators, such as norepinephrine, serotonin, and acetylcholine have also been implicated in regulating both developmental plasticity and LTP/LTD. There are many potential levels of interaction between neuromodulators and plasticity. Ion channels are substrates for modulation in many cell types. We discuss examples of modulation of voltage-gated Ca2+ channels and Ca(2+)-dependent K+ channels and the consequences for neocortical pyramidal cell firing behaviour. At the time when developmental plasticity is most evident in rat cortex, the substrate for modulation is changing as the densities and relative proportions of various ion channels types are altered during ontogeny. We discuss examples of changes in K+ and Ca2+ channels and the consequence for modulation of neuronal activity.

Environmental influence on gene expression and recovery from cerebral ischemia.

Abstract: An emerging concept in neurobiology is that the adult brain retains a capacity for plasticity and functional reorganization throughout the life span. Experimental data from electrophysiological, morphological and behavioral studies have documented experience dependent plasticity in the intact and injured adult brain. Neuroimaging clinical studies indicate altered post stroke functional activation patterns, usually including activation of the intact hemisphere. However, there is some disagreement regarding their functional significance and longitudinal studies correlating outcome and activation pattern are needed to solve some controversies. Postoperative housing of rats in activity stimulating environment after ligation of the middle cerebral artery significantly enhances outcome. Gene expression for brain derived neurotrophic factor and Ca2+/calmodulin-dependent protein kinase II, two substances with potential role in brain plasticity, show different patterns in animals housed in standard and in enriched environment. The functional significance of altered gene expression needs to be evaluated.

On nature and limits of cortical developmental plasticity after an early lesion, in a child

Abstract: MS is a little girl who suffered severe, bilateral destruction of her primary visual areas at six weeks, after premature birth at 30 weeks. Between the ages of 4.5 and 5.5 years she partially recovered different aspects of visual function, and, in particular, the ability to segregate figures from background, based on texture cues. The recovery might have been due to the compensatory role of the remaining visual areas that could have acquired response properties similar to those of the primary visual areas. This is not supported by the available FMRI (functional magnetic resonance imaging) responses to visual stimuli. Instead, abnormalities in the pattern of stimulus-induced changes of interhemi-spheric EEG-coherence in this patient suggest that her visual callosal connections, and possibly other cortico-cortical connections have re-organized abnormally. Since cortico-cortical connections, including the callosal ones appear to be involved in perceptual binding and figure-background segregation, their reorganization could be an important element in the functional recovery after early lesion, and/or in the residual perceptual impairment.

Restriction of developmental potential during divergence of the enteric and sympathetic neuronal lineages

Abstract: In the peripheral nervous system, enteric and sympathetic neurons develop from multipotent neural crest cells. While local environmental signals in the gut and in the region of the sympathetic ganglia play a role in the choice of cell fate, little is known about the mechanisms that underlie restriction to specific neuronal phenotypes. We investigated the divergence and restriction of the enteric and sympathetic neuronal lineages using immuno-isolated neural crest-derived cells from the gut and sympathetic ganglia. Analysis of neuronal and lineage-specific mRNAs and proteins indicated that neural crest-derived cells from the gut and sympathetic ganglia had initiated neuronal differentiation and phenotypic divergence by E14.5 in the rat. We investigated the developmental potential of these cells using expression of tyrosine hydroxylase as a marker for a sympathetic phenotype. Tyrosine hydroxylase expression was examined in neurons that developed from sympathetic and enteric neuroblasts under the following culture conditions: culture alone; coculture with gut monolayers to promote enteric differentiation; or coculture with dorsal aorta monolayers to promote noradrenergic differentiation. Both enteric and sympathetic neuroblasts displayed developmental plasticity at E14.5. Sympathetic neuroblasts downregulated tyrosine hydroxylase in response to signals from the gut environment and enteric neuroblasts increased expression of tyrosine hydroxylase when grown on dorsal aorta or in the absence of other cell types. Tracking of individual sympathetic cells displaying a neuronal morphology at the time of plating indicated that neuroblasts retained phenotypic plasticity even after initial neuronal differentiation had occurred. By E19.5 both enteric and sympathetic neuroblasts had undergone a significant loss of their developmental potential, with most neuroblasts retaining their lineage-specific phenotype in all environments tested. Together our data indicate that the developmental potential of enteric and sympathetic neuroblasts becomes restricted over time and that this restriction takes place not as a consequence of initial neuronal differentiation but during the period of neuronal maturation. Further, we have characterized a default pathway of adrenergic differentiation in the enteric nervous system and have defined a transient requirement for gut-derived factors in the maintenance of the enteric neuronal phenotype.

Plasticity of Developmental Timing as the Underlying Cause of High Speciation Rates in Ammonoids

Abstract: Rapid diversification of clades within a restricted geographic area is fairly common, and has been well studied as a model of adaptive radiation The monophyletic clades produced by this type of event have been called “species flocks” An investigation of the Cenomanian radiation of acanthoceratid ammonites in the North American Western Interior Seaway reveals that this clade shows all the characteristics of a species flock: the acanthoceratid genera are speciose and diversified rapidly, and many of the species are geographically restricted within the Western Interior, possibly due to environmental barriers A cladistic analysis shows many true polytomies, a high autapomorphy to synapomor- phy ratio, and much parallelism, all reflecting rapid diversification from a single ancestral lineage These ammonites also show pronounced plasticity of developmental timing Most differences in morphology among taxa are due to small changes in developmental timing, and an unusually high number of progenic dwarf spinoff taxa occur in this clade, indicating that larger-scale changes in ontogenetic timing are also common It seems, then, that the developmental program of this ammonite clade was exceedingly labile during its radiation This plasticity may have allowed the clade to radiate so rapidly and profusely As developmental plasticity may be a characteristic of ammonoids as a whole, this internal factor, rather than sensitivity to external environmental conditions, may be the root cause of high speciation rates in ammonoids

Role of neurotrophins in neural plasticity: what we learn from the visual cortex.

Abstract: A role for neurotrophins in regulating cortical developmental plasticity has clearly emerged in these last years. In this review we first present a summary of the early data on the action of NGF in visual cortical development and plasticity in the rat and of the actions of the other neurotrophins in the visual cortex of other mammals. In addition, in order to clarify the differerences in the results obtained with the various neurotrophins in different animal preparations we also report new data on the action of NGF, BDNF, NT3 and NT4 in the same preparation. namely the visual cortex of the rat. We discuss old and new results in a physiological model where different neurotrophins play different roles in regulating visual cortical development and plasticity by acting on different neural targets, such as LGN afferents, intracortical circuitry and subcortical afferents and propose a tentative scheme summarizing these actions.

Plasticity in Nerve Cell Function

Abstract: Preface 1. Formation of neural networks 2. Developmental plasticity of neuronal elements 3. Synaptic plasticity 4. Aging and neuronal functions 5. Glia and neuronal plasticity 6. Common features in the mechanisms of different forms of neuronal plasticity Bibliography

The role of neurotrophins in developmental cortical plasticity.

Abstract: Purpose - It has been proposed that experience dependent maturation and reorganization in the neocortex might be based on the activity dependent competition between different sets of axons for growth related molecules such as neurotrophins. In the present study we tested this hypothesis by examination of the effects of external administration of NGF and BDNF on the experience dependent rearrangement of thalamo-cortical connections after monocular deprivation (MD) in the developing cam visual cortex. Methods - The visual cortices of kittens were infused intracortically either with BDNF, NGF or cytochrome C while the animals were subjected to MD for one week during the peak of the critical period (postnatal day 26 to postnatal day 40). Subsequently cortical neuronal responses were assessed with optical (optical imaging of intrinsic signals) and single unit recording techniques. Results - In control hemispheres treated with cytochrome C, MD had caused the expected shift of OD towards the normal eye. Also hemispheres treated with NGF exhibited a strong shift of OD towards the open eye. However, in the BDNF infused hemispheres OD had shifted towards the deprived eye in a zone extending 2.5-3 5 mm from the infusion cannula and neurons had lost their orientation selectivity. In an adjacent transition zone both eyes activated the cortex equally well and responses were again tuned for orientation and at still larger distances OD was shifted towards the normal eye. Conclusions - The present data support the concept of an involvement of neurotrophins in cortical plasticity. However, our observations suggest for both neurotrophins, NGF and BDNF, a more complex role in the developing neocortex than serving simply as the substrate of an activity dependent competition process within the visual cortex. Moreover, the outcome of our study indicates strong differences between BDNF and NGF concerning their involvement and locus of action in developmental plasticity.

Neural activity and immediate early gene expression in the cerebral cortex

Abstract: Immediate early gene (IEG) expression is dynamically regulated in brain neurons, in response to natural activity, and linked to neural plasticity. Because of the demonstrated importance of synaptic activity in neuronal function and development, it is anticipated that IEGs contribute to adult and developmental cortical plasticity. The IEG response includes proteins that function as transcription factors, as well as enzymes and growth factor proteins that can directly modify neuronal and synaptic function. An understanding of the mechanistic contribution of the IEG response to neuronal plasticity will provide information not only about basic developmental processes, and their disturbances in mental retardation, but may also contribute to new diagnostic and therapeutic approaches for these developmental disorders. MRDD Research Reviews 1999;5:41–50. © 1999 Wiley-Liss, Inc.

Neural recognition molecules and synaptic plasticity

Abstract: Recent studies of neural recognition molecules have revealed similarities between their functions during ontogenetic development and in neural plasticity in the adult. Observations both at the cellular level in vitro and at the behavioural level in vivo suggest that altered recognition molecule expression can lead to changes in synaptic efficacy, and alterations in synaptic function in turn evoke changes in recognition molecule expression. These changes can manifest themselves as morphological alterations and modulations of the synapse's signal transduction machinery.

Computational study of experience-dependent plasticity in adult rat cortical barrel-column.

Abstract: We model experience-dependent plasticity in the adult rat S1 cortical representation of the whiskers (the barrel cortex) which has been produced by trimming all whiskers on one side of the snout except two. This manipulation alters the pattern of afferent sensory activity while avoiding any direct nerve damage. Our simplified model circuitry represents multiple cortical layers and inhibitory neurons within each layer of a barrel-column. Utilizing a computational model we show that the evolution of the response bias in the barrel-column towards spared whiskers is consistent with synaptic modifications that follow the rules of the Bienenstock, Cooper and Munro (BCM) theory. The BCM theory postulates that a neuron possesses a dynamic synaptic modification threshold, M, which dictates whether the neuron's activity at any given instant will lead to strengthening or weakening of the synapses impinging on it. However, the major prediction of our model is the explanation of the delay in response potentiation in the layer-IV neurons through a masking effect produced by the thresholded monotonically increasing inhibition expressed by either the logarithmic function, h.x/D log. 1+ x/, or by the power function,h.x/D x 0:8 0:9 , where is a constant. Furthermore, simulated removal of the supragranular layers (layers II/III) reduces plasticity of neurons in the remaining layers (IV-VI) and points to the role of noise in synaptic plasticity.

Stability of behavioral traits within the framework of neural plasticity

Abstract: Lifelines supports the theme that behavioral development is a fluid, life-long phenomenon. In contrast, many emotional and cognitive traits are subject to strong genetic influence, and are highly stable over many years. The manner in which neuroplasticity and trait stability cooccur needs to be modeled. An outline of such a model is provided to promote discussion of this complex issue.