Showing papers on "Developmental plasticity published in 1992"

Activity-dependent decrease in NMDA receptor responses during development of the visual cortex

Abstract: Plasticity of the developing visual system has been regarded as the best model for changes of neuronal connections under the influence of the environment. N-methyl-D-aspartate (NMDA) receptors are crucial for experience-dependent synaptic modifications that occur in the developing visual cortex. NMDA-mediated excitatory postsynaptic currents (EPSCs) in layer IV neurons of the visual cortex lasted longer in young rats than in adult rats, and the duration of the EPSCs became progressively shorter, in parallel with the developmental reduction in synaptic plasticity. This decrease in NMDA receptor-mediated EPSC duration is delayed when the animals are reared in the dark, a condition that prolongs developmental plasticity, and is prevented by treatment with tetrodotoxin, a procedure that inhibits neural activity. Application of L-glutamate to outside-out patches excised from layer IV neurons of young, but not of adult, rats activated prolonged bursts of NMDA channel openings. A modification of the NMDA receptor gating properties may therefore account for the age-dependent decline of visual cortical plasticity.

Heterochronic developmental plasticity in larval sea urchins and its implications for evolution of nonfeeding larvae.

Abstract: Preexisting developmental plasticity in feeding larvae may contribute to the evolutionary transition from development with a feeding larva to nonfeeding larval development. Differences in timing of development of larval and juvenile structures (heterochronic shifts) and differences in the size of the larval body (shifts in allocation) were produced in sea urchin larvae exposed to different amounts of food in the laboratory and in the field. The changes in larval form in response to food appear to be adaptive, with increased allocation of growth to the larval apparatus for catching food when food is scarce and earlier allocation to juvenile structures when food is abundant. This phenotypic plasticity among full siblings is similar in direction to the heterochronic evolutionary changes in species that have greater nutrient reserves within the ova and do not depend on particulate planktonic food. This similarity suggests that developmental plasticity that is adaptive for feeding larvae also contributes to correlated and adaptive evolutionary changes in the transition to nonfeeding larval development. If endogenous food supplies have the same effect on morphogenesis as exogenous food supplies, then changes in genes that act during oogenesis to affect nutrient stores may be sufficient to produce correlated adaptive changes in larval development.

Developmental plasticity in neural circuits controlling birdsong: sexual differentiation and the neural basis of learning.

Abstract: In many species of passerine songbirds, males learn their song during defined periods of life. Female song in often reduced or absent, as are the brain regions controlling song. Sexual differences in the brain arise because of the action of sex steroids, which trigger the formation of some neural pathways (especially the pathway from the higher vocal center to the robust nucleus) and prevent the atrophy of others in males. These neural changes occur during periods of developmental song learning and can recur during periods of learning in adult birds. The process of learning is correlated with major increases or decreases in the number of neurons in specific neuronal populations, suggesting that the formation or loss of specific neural pathways regulates the ability to learn. Species differences in sexual differentiation and learning allow informative cross-species comparisons of neural structure and behavior. © 1992 John Wiley & Sons, Inc.

A role for glial cells in activity-dependent central nervous plasticity? Review and hypothesis.

Abstract: Activity-dependent plasticity relies on changes in neuronal transmission that are controlled by coincidence or noncoincidence of presynaptic and postsynaptic activity. These changes may rely on modulation of neural transmission or on structural changes in neuronal circuitry. The present overview summarizes experimental data that support the involvement of glial cells in central nervous activity-dependent plasticity. A role for glial cells in plastic changes of synaptic transmission may be based on modulation of transmitter uptake or on regulation of the extracellular ion composition. Both mechanisms can be initiated via neuronal-glial information transfer by potassium ions, transmitters, or other diffusible factor originating from active neurons. In addition, the importance of changes in neuronal circuitry in many model systems of activity-dependent plasticity is summarized. Structural changes in neuronal connectivity can be influenced or mediated by glial cells via release of growth or growth permissive factors on neuronal activation, and by active displacement and subsequent elimination of axonal boutons. A unifying hypothesis that integrates these possibilities into a model of activity-dependent plasticity is proposed. In this model glial cells interact with neurons to establish plastic changes; while glial cells have a global effect on plasticity, neuronal mechanisms underlie the induction and local specificity of the plastic change. The proposed hypothesis not only explains conventional findings on activity-dependent plastic changes, but offers an intriguing possibility to explain several paradoxical findings from studies on CNS plasticity that are not yet fully understood. Although the accumulated data seem to support the proposed role for glial cells in plasticity, it has to be emphasized that several steps in the proposed cascades of events require further detailed investigation, and several "missing links" have to be addressed by experimental work. Because of the increasing evidence for glial heterogeneity (for review see Wilkin et al., 1990) it seems to be of great importance to relate findings on glial populations to the developmental stage and topographical origin of the studied cells. The present overview is intended to serve as a guideline for future studies and to expand the view of "neuro" physiologists interested in activity-dependent plasticity. Key questions that have to be addressed relate to the mechanisms of release of growth and growth-permissive factors from glial cells and neuronal-glial information transfer. It is said that every complex problem has a simple, logical, wrong solution. Future studies will reveal the contribution of the proposed simple and logical solution to the understanding of central nervous plasticity.

Brain aging and neuronal plasticity

Abstract: The aging of any system of our organism can be quantified by the decrease in its performance. When the system performance is plotted versus age, a monotonically decreasing function can be obtained after maturity. The aging of the central nervous system (CNS) cannot be assessed in a similar fashion, since no single performance represents the overall CNS function. The best characterization of the decreased capabilities of the CNS observed in aged humans is probably the reduction in creativity, a highly characteristic but not easily quantifiable feature of the human brain. For no other system in the human organism does there exist such great interindividual variability in age-induced reduction in performance as in the CNS. It has been shown that from maturity to old age all the other systems of the human organism have at least a 50% decrease in performance, with no reported cases of increase in performance. On the contrary, some individuals reach the highest intellectual performance, in terms of creative power, in old age. A very famous case is that of the Greek tragedian Sophocles, who wrote “Oedipus at Colonus” when he was more than eighty years old (Cicero, De senecrute, VII 22). An intriguing aspect of CNS aging is the lack of a strict correlation between intellectual impairment and neuropathological changes.’ Except for the most extreme cases, it is not possible to foresee the neuropathological state of a subject by neuropsychological examination. This lack of correlation may have different explanations. One explanation takes into account that neurons are organized in neuronal networks according to hierarchical principles, with the highest-ranking neurons having the lowest redundancy. Thus, if the aging processes hit this special class of neurons, a marked intellectual deficit may be observed in the presence of scarce neuropathological damage. On the other hand, if the aging processes hit low-ranking, highly redundant neurons, little or no intellectual deficit may occur in the presence of diffuse histological damage.*

The critical period for experience-dependent plasticity in a system of binocular visual connections in Xenopus laevis : its temporal profile and relation to normal developmental requirements

Abstract: A commissural system of 'intertectal' connections in Xenopus mediates the registration of binocular visual maps at the midbrain optic tectum. Following surgical eye rotation in larval animals, the system can completely alter its pattern of connectivity to restore binocular visual registration at the tectum. This experimentally induced plasticity is known to require visual experience and thought to be subject to an age-related restriction: eye rotation in adult animals is reported to provoke no subsequent intertectal alteration. In this paper we describe the detailed age-dependence of this plasticity. One eye was rotated in 238 animals of various developmental stages between mid-larval and adult life. At each age, different animals received rotations of different sizes, ranging from 20 to 180 degrees. The pattern of intertectal connectivity was mapped electrophysiologically 1 - 2 years postoperatively. A 'critical' period was defined around the time of metamorphosis: the vast majority of animals receiving a rotation in larval life (up to approximately 2 weeks before metamorphic climax) showed altered intertectal connections, whereas none of the animals operated upon at 3 months or more postmetamorphosis displayed the plasticity. At intervening ages, altered intertectal connections were found only in response to progressively smaller eye rotations. The profile of this critical period was further shown to mirror temporal features of the changes in eye position that occur in Xenopus as natural consequences of head growth, and which themselves impose a normal developmental requirement for intertectal plasticity. We conclude that the capacity of the Xenopus intertectal system for plasticity in response to abnormal experience undergoes a progressive age-dependent decline, and that the profile of this decline is delimited by normal requirements.

The Critical Period for Experience-dependent Plasticity in a System of Binocular Visual Connections in Xenopus laevis: Its Extension by Dark-rearing.

Abstract: Following surgical rotation of an eye, the Xenopus 'intertectal' system is capable of a vision-dependent alteration of its connectivity, that restores spatial registration of binocular maps on the optic tectum. In the preceding paper (Keating and Grant, Eur. J. Neurosci., 4, 27 - 36, 1992), we reported that this capacity undergoes a progressive, age-dependent restriction during a critical period around the time of metamorphosis, so that rotations produced in animals aged >/=3 months postmetamorphosis normally evoke no such alteration of the system. Here we examine whether this restriction is rigidly age-dependent or whether vision can influence its profile. We report that in animals dark-reared from embryonic stage 35 through the critical period to 3 months, 1 year or even 2 years after metamorphosis, rotations instituted at those ages now result in intertectal reorganization if a period of normal vision is allowed after the operation. Similarly, intertectal alteration was also seen in animals eye-rotated at larval stage 58, then dark-reared just for the duration of the critical period, and subsequently returned, at 3 months of age, to a normal visual environment. We conclude, therefore, that the normal developmental restriction in the plasticity of the Xenopus intertectal system is not strictly age-dependent, but that vision contributes to the process by activating the underlying plasticity mechanisms.

Brain plasticity and regeneration.

Abstract: Brain plasticity includes the enormous changes of normal prenatal and postnatal development, responses to normal experience such as the springtime reemergence of bird song, and responses to injury. This broad view of plasticity brings together the large and growing fields of developmental neuroscience, learning and memory, and responses to injury. Such a synthetic view is essential now that these fields are being elucidated at cellular and molecular levels. The major stages of normal brain development are very similar to those of plasticity induced by experience. Particular cellular or subcellular de,.. tails are similar, depending on the specific case. Importantly, these common steps are the very ones we most need to understand if the outcome of brain and spinal cord injury is to be improved. Knowledge of brain plasticity will be the basis for innovative treatmenf of such injuries. Relevant mechanisms reviewed here include chemical stimulation of receptors, regulation of gene expression in surviving cells, gene introduction by viral or cellular vectors, cell-cell interactions such as guidance of axons, and replacing neurons lost by injury. Increasing knowledge of plasticity and its application to therapy offers promising approaches for improving the outcome of cerebral and spinal injury, making optimism unavoidable.