Showing papers on "Developmental plasticity published in 1996"

Experience-Dependent Plasticity of Binocular Responses in the Primary Visual Cortex of the Mouse

Abstract: An activity-dependent form of synaptic plasticity underlies the fine tuning of connections in the developing primary visual cortex of mammals such as the cat and monkey. Studies of the effects of manipulations of visual experience during a critical period have demonstrated that a correlation-based competitive process governs this plasticity. The cellular mechanisms underlying this competition, however, are poorly understood. Transgenic and gene-targeting technologies have led to the development of a new category of reagents that have the potential to help answer questions of cellular mechanism, provided that the questions can be studied in a mouse model. The current study attempts to characterize a developmental plasticity in the mouse primary visual cortex and to demonstrate its relevance to that found in higher mammals. We found that 4 d of monocular lid suture at postnatal day 28 (P28) induced a maximal loss of responsiveness of cortical neurons to the deprived eye. These ocular dominance shifts occurred during a well-defined critical period, between P19 and P32. Furthermore, binocular deprivation during this critical period did not decrease visual cortical responses, and alternating monocular deprivation resulted in a decrease in the number of binocularly responsive neurons. Finally, a laminar analysis demonstrated plasticity of both geniculocortical and intracortical connections. These results demonstrate that an activity-dependent, competitive form of synaptic plasticity that obeys correlation-based rules operates in the developing primary visual cortex of the mouse.

Quantitative aspects of synaptogenesis in the rat barrel field cortex with special reference to GABA circuitry

Abstract: The postnatal establishment of cortical connectivity was studied by estimating the number (numerical density, synapse-to-neuron ratio, and total number) of the overall synaptic population and its distribution into gamma-aminobutyric acid (GABA)-immunopositive and GABA-immunonegative synaptic contacts in the developing rat somatosensory cortex. These numerical data were obtained using the unbiased disector method in combination with GABA postembedding immunocytochemistry. The numerical density of both synaptic populations was low in the early postnatal period (postnatal days 5 and 10, P5, P10) after which it abruptly increased between P10 and P15 to approach adult values. However, since cortical volume continues to increase after this age, the number of synapses per neuron and the total number of synapses reached adult values only by P30. There was no evidence of overproduction of either GABA or non-GABA synapses. Direct comparison between the two synaptic populations revealed a similar developmental pattern with the exception of the period around P20 when the production of GABA synapses slowed down. Thus, while the formation of non-GABA synapses proceeded in a continuous manner throughout the first month of life, GABA synapse production was accomplished in two consecutive waves. We suggest that the second delayed wave of GABA synapse formation is related to the great developmental plasticity of the cortical inhibitory system.

Requirement for α-CaMKII in Experience-Dependent Plasticity of the Barrel Cortex

Abstract: The mammalian sensory neocortex exhibits experience-dependent plasticity such that neurons modify their response properties according to changes in sensory experience. The synaptic plasticity mechanism of long-term potentiation requiring calcium-calmodulin-dependent kinase type II (CaMKII) could underlie experience-dependent plasticity. Plasticity in adult mice can be induced by changes in the patterns of tactile input to the barrel cortex. This response is strongly depressed in adult mice that lack the gene encoding α-CaMKII, although adolescent animals are unaffected. Thus, α-CaMKII is necessary either for the induction or for the expression of plasticity in adult mice.

Rapid and opposite effects of BDNF and NGF on the functional organization of the adult cortex in vivo

Abstract: THE adult cortex is thought to undergo plastic changes that are closely dependent on neuronal activity (reviewed in ref. 1), although it is not yet known what molecules are involved. Neurotrophins and their receptors have been implicated in several aspects of developmental plasticity, and their expression in the adult cortex suggests additional roles in adult plasticity. To examine these potential roles in vivo, we used intrinsic-signal optical imaging to quantify the effects of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) on the functional representation of a stimulated whisker in the 'barrel' subdivision of the rat somatosensory cortex. Topical application of BDNF resulted in a rapid and long-lasting decrease in the size of a whisker representation, and a decrease in the amplitude of the activity-dependent intrinsic signal. In contrast, NGF application resulted in a rapid but transient increase in the size of a representation, and an increase in the amplitude of the activity-dependent intrinsic signal. These results demonstrate that neurotrophins can rapidly modulate stimulus-dependent activity in adult cortex, and suggest a role for neurotrophins in regulating adult cortical plasticity.

Leaf developmental plasticity of Ranunculus flabellaris in response to terrestrial and submerged environments

Abstract: Environmentally induced developmental plasticity is characteristic of many heterophyllous semiaquatic species, including Ranunculus flabellaris. Underwater shoots of this species form leaves with e...

Possible involvement of neuromodulatory systems in cortical Hebbian-like plasticity

Abstract: Plasticity of neuronal covariances (functional plasticity) is controlled by behavior (Ahissar et al (1992) Science 257, 1412–1415). Whether this behavioral control involves neuromodulatory systems was tested by examining the effect of acetylcholine (ACh) and noradrenaline (NE) on functional plasticity in anesthetized animals and by comparing the effects of these neuromodulators in an anesthetized preparation to that of behavior in awake animals. Local iontophoretic applications of these drugs during manipulations of activity covariance in guinea pig auditory cortex did not mimic the behavioral control of functional plasticity that was previously observed in awake monkeys. Thus, the hypotheses according to which these neuromodulators control functional plasticity independent of their concentration and time of release were not supported by our data. The significant plasticity induced nevertheless, by some of the conditionings in the presence of ACh and NE, suggests that factors, other than those that were experimentally controlled, could regulate this plasticity. These factors could be among others the timing of drug(s) applications relative to the conditioning time, the local concentrations of the drug(s) and/or the site of application with respect to the relevant synapses.

Motor learning and synaptic plasticity in the cerebellum

Abstract: For reasons I have never understood, some students of the cerebellum have been unwilling to accept the now overwhelming evidence that the cerebellum exhibits lasting synaptic plasticity and plays an essential role in some forms of learning and memory. With a few exceptions (e.g., target article by SIMPSON et al.) this is no longer the case, as is clear in the excellent target articles on cerebellar LTD and the excellent target review by HOUK et al. [CREPEL et al.; HOUR et al.; KANO; LINDEN; SIMPSON et al.; SMITH; VINCENT]

Axonal Processes and Neural Plasticity. II: Adult Somatosensory Maps

Abstract: Following our recent presentation of an axonal process sprouting and retraction framework for ocular dominance column formation, we now apply it, unchanged, to address issues of adult somatosensory map plasticity. Specifically, we model the rearrangement of S-I in adult rodents following denervation of a row of vibrissae, and the rearrangement of area 3b in adult monkeys following hyperstimulation of a digit. While we do not attempt to capture the rapid changes which occur as the result of unmasking or potentiating existing connections, we demonstrate that axonal process sprouting and retraction is a possible mechanism mediating many of the long-term changes induced by anomalous peripheral activity. A significant feature of our framework, demonstrated by this study, is that it can account for plasticity in both developing and mature systems, and in different sensory modalities. In contrast, synapse-specific Hebbian models with synaptic normalization, which employ anatomically fixed connections capable of changes in efficacy, may not be able to account for both developmental and adult plasticity without the form of the imposed normalization, which enforces competition between afferents, being changed.

Protein and RNA synthesis-dependent and -independent LTPs in developing rat visual cortex.

Abstract: Multiple forms of synaptic potentiation have been described, but their involvement in development versus learning is unknown. To address this, we examined whether long-term potentiation (LTP) in visual cortex requires protein or RNA synthesis using slice preparations. Theta-burst stimulation of white matter induced two distinct types of LTP in layer 4. A slowly developing LTP, preferentially induced in juveniles, was blocked by protein and RNA synthesis inhibitors and was L-type calcium channel dependent. A quickly developing LTP, induced in juveniles and adults, was independent of macromolecular synthesis and required N-methyl-D-aspartate receptor activation. Thus, slow LTP might account for developmental plasticity in visual cortex including the activity-dependent refinement of neural circuitry while fast LTP might underlie the changes in synaptic strength that may participate in visual learning and memory.

Epigenetic modifications and gene silencing in plants.

Abstract: During the development of plants, meristems and organ primordia become progressively committed to form specific and definite structures. This process, called determination, results from stable changes in phenotype that persist in the absence of the agent that originally induced the change. As a consequence, parts of an organism can “remember” their past, and this permits new formation of structures. Nevertheless, plants also show remarkable developmental plasticity. The shape and size of organs are strongly influenced by the environment, and plants have a pronounced capacity for regeneration. The developmental plasticity of determined structures illustrates the important point that stable changes are not necessarily irreversible. Determination is a relative process: Developmental states stable in one environment are not necessarily stable in some other environment (Meins and Wenzler 1986). Little is known about the molecular mechanisms underlying stable reversible changes in plants. Recent studies show that multiple copies of transgenes introduced into plant cells can interact with one another or with homologous host genes in trans, resulting in the inactivation of expression of both genes. This phenomenon, called silencing (Jorgensen 1992) or cosuppression (Napoli et al. 1990), is of particular interest because it provides well-defined experimental systems for investigating the molecular basis for stable reversible changes. The aim of this chapter is to call attention to the similarities between stable changes in plant development and gene silencing and to propose general biochemical switch models that can account for many features of both forms of variation. THE CONCEPT OF EPIGENETIC CHANGE Stable Changes in...

Brain plasticity: influence of environment.

Abstract: T he following reprinted article is the first of two classic works included in our series that involve an area of great importance to neuropsychiatry: the study of how environment and life experience influence brain structure. The study of brain plasticity is crucial to understanding the biology of learning and memory, as well as the potential of the brain to recover from injury. In this issue we feature a study by Drs. Edward Bennett, Marian Diamond, David Krech, and Mark Rosenzweig of the University of California, Berkeley, which demonstrates that rats living in an enriched environment have an increase in brain weight and thickness of the cortex and an increase in total brain acetylcholinesterase activity compared with littermates living in more restricted settings.’ In a subsequent issue we will reprint one of several landmark studies by David Hubel and Torsten Wiesel, who in the early 1960s demonstrated that the cytoarchitectune of the visual cortex is greatly responsive to manipulations of visual stimulation during early development. Mark Rosenzweig, in a recent historical review of the search for the biological basis of brain plasticity,2 dates the first controlled study of environmental experience and brain structure to the eighteenth century. Michele Malacame (1744-1816), an Italian anatomist, took a pair of dogs from the same litter and several pairs of birds from clutches of eggs and gave one in each pair extensive training over several years. Examination of the brains showed that animals with intensive training had more folds in the cerebellum. Years later, Charles Darwin observed that domesticated animals had smaller brains than their wild counterparts.3 He speculated that this was due in part to a relative impoverishment of life experience brought on by domestication.4 Santiago Ram#{243}n y Cajal, the great Spanish neurohistologist, believed that learning and enriched mental experience increased the number of neuronal branches.5 Donald Hebb, who was a major influence on Dr. Rosenzweig, reported that animals raised in an enriched environment performed better on multiple learned tasks.6 Hubel and Wiesel7 showed that depriving kittens of visual stimulation in one or both eyes results in structural change to the visual cortex. Drs. Rosenzweig, Knech, and Bennett in the mid-1950s became interested in the correlation between problemsolving ability in animals and brain acetylcholinestenase (AChE) activity.8 To their surprise, they found that cortical AchE activity varied as a function of the intensity of training their rats had received.9 Out of practical and economic considerations, they shifted their experimental paradigm from intensive training to a comparison of enriched versus restricted environments. They recruited Dr. Diamond to enhance their anatomic studies. Since they were interested in measuring AchE activity per unit weight of brain mass, they were able to discover something even more remarkable. The animals raised in enriched environments had a small but a reliable increase in brain weight compared with littermates raised in restricted environments.’0 These researchers subsequently pursued many replication and control studies, described in their article reprinted here, that showed that this finding was not an artifact of isolation stress, differential handling, or locomotor activity. In addition, they found that this effect occurred in animals at all points of the life cycle. Their further studies also showed effects of experience on detailed anatomic measures such as numbers of dendritic spines, nerve cell volume, and numbers of glial cells. Dr. Bennett, in a telephone interview, said that at the time of this study few people believed that the brain would respond like a muscle with usage. And Dr. Rosenzweig affirmed that “training can modulate the genetic given.” Many other groups have replicated their findings, including Volkmar and Greenough at the University of Illinois, Champaign, who demonstrated that animals raised in enriched environments have greater dendritic branching in the occipital cortex.” Currently, the study of macroscopic and molecular structural changes associated with experience, learning, and memory is a large and fascinating area of

The plasticity of systemic brain mechanisms

Abstract: Mechanisms of plasticity of the main components (dominant motivation and reinforcement) of systemic behavioural act organisation are considered. It is shown that dominant motivation changes different properties of brain neurones including their specific sensitivity to neuromediators and neuropeptides. Reinforcement in its turn modifies the properties of brain neurones which take part in dominant motivation. The foregoing reinforcement influences the modification of genetic apparatus of neurones involved in dominant motivation and, as a consequence, they begin to express specific information molecules under the influence of dominant motivation in the subsequent formation of the corresponding drive. The information molecules organise a corresponding behaviour. Plasticity properties of brain neurones are mostly revealed in conflict situations leading to emotional stress. Reorganisation of chemical integration of limbic-reticular neurones takes place under emotional stress. Oligopeptides play the leading role in these processes. It is shown that oligopeptides are able to compensate the functions of damaged limbic-reticular brain structures.

Developmental processes and the pathophysiology of mental retardation

Abstract: Some of the known causes of mental retardation (MR) include genetic abnormalities, exposure to toxins, many types of infections, malnutrition, brain trauma, and even extreme postnatal neglect. The developing brain is vulnerable to these insults during all the identifiable stages of brain development. Gastrulation leads to the formation of the three germ layers, and neurulation leads to the formation of the central and peripheral nervous systems. Cells formed in these nervous systems migrate from their site of origin to their final position in the brain and periphery. They then differentiate into structures and cells with the final functional properties of nerve cells during prenatal and postnatal activity-dependent periods. All reported causes of MR also produce other types of impairments, which may include physical, neurologic, or psychiatric manifestations and disabilities. The authors suggest that if the biological basis of normal learning, memory, and adaptive behavior can be reduced to cellular events, regulation of synaptic strength would be the most fundamental basis of neural plasticity and learning. Thus, understanding conditions or events that impair or delay development of brain mechanisms for plasticity, learning, and memory is an important first step in understanding the conditions that prevent their development. This article focuses on the particular aspects of neuroembryology, differentiation, and synaptic modification that are particularly vulnerable to developmental insults that cause MR. The most effective types of behavioral and other interventions in the future may be improved by knowledge of the rules that regulate the development of brain plasticity mechanisms in experimental animals. © 1997 Wiley-Liss, Inc.