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Showing papers on "Developmental plasticity published in 1989"


Journal ArticleDOI
TL;DR: The results indicate that the presence of a transplant prolongs the critical period for developmental plasticity of the CST, and suggest that both environmental and neuronal factors interact to regulate the response of immature CS neurons to injury.
Abstract: The corticospinal tract (CST) of the rat undergoes a prolonged period of postnatal development. Lesions of the presumptive CST pathway at birth are followed by the aberrant rerouting of the developing corticospinal axons around the lesion site through adjacent undamaged CNS tissue. This developmental plasticity becomes severely restricted by 5-6 days of age, so the axons are no longer capable of growth around the site of injury. The aim of the current study was to determine whether altering the environment at the site of injury by filling the lesion with transplanted fetal spinal cord tissue could prolong the critical period for developmental plasticity of the corticospinal pathway. The spinal cord was damaged (overhemisection) at three stages in the development of the corticospinal (CS) pathway: 1) prior to the arrival of CS axons, 2) after the axons elongated through the cord but prior to synaptogenesis, and 3) after both axonal elongation and synaptogenesis were completed. One to 9 months later, anterograde neuronal tracing with horseradish peroxidase was used to assess the growth of the corticospinal pathway with or without a fetal transplant at the site of injury, and the pattern of labeling was compared with that observed in adult nonlesioned control animals. Our results indicate that the presence of a transplant prolongs the critical period for developmental plasticity of the CST. Transplants elicited growth of CST axons throughout the postnatal period examined. CST axons damaged prior to synaptogenesis exhibited more robust growth than those lesioned after synaptogenesis had been completed. These results suggest that both environmental and neuronal factors interact to regulate the response of immature CS neurons to injury.

129 citations


Journal ArticleDOI
TL;DR: Way in which receptors, key components of signal propagation through a synapse, can mediate changes in that propagation is described, focusing on neuronal receptors.
Abstract: This article describes ways in which receptors, key components of signal propagation through a synapse, can mediate changes in that propagation. Changes occur at four levels: in the signal-transducing capability of a single receptor molecule, in the number of receptors per cell, in the subcellular placement of receptor molecules, and in the cytoarchitecture of receptor-rich regions. The ability of receptors to shift between different desired states is called plasticity, and such shifts can be long-lived as well as transient. In this article we focus on neuronal receptors, although key findings from a variety of cell systems are reported. Neuronal receptor plasticity may have a special role in the assembly as well as the adaptability of the nervous system.

65 citations


Journal ArticleDOI
TL;DR: Although hypometabolism exists in the cerebellum, it is not clear why there are no cerebellar symptoins and it may be the case that hypometabolic dysfunction represents a different process than a frank lesion of the cerebelum.
Abstract: evoked potential occurred which &dquo;recovered&dquo; in amplitude over time. In addition to changes in electrophysiological parameters, remote metabolic perturbations have been described by Baron. Following frontal cortex injury, reduced metabolic activity exists predominantly in the cerebellum contralateral to the injury. This disturbance was presumably mediated via injury to the corticopontocerebellar pathway. Although hypometabolism exists in the cerebellum, it is not clear why there are no cerebellar symptoins. It may be the case that hypometabolic dysfunction represents a different process than a frank lesion of the cerebellum.

20 citations



Journal ArticleDOI
TL;DR: Although this book began as a summary of a meeting held by the Society of Experimental Biology, the topic became of such interest that the chapters were expanded to form bona fide reviews, and the list of contributors was expanded to include some workers not at the original meeting.
Abstract: Although this book began as a summary of a meeting held by the Society of Experimental Biology, the topic became of such interest that the chapters were expanded to form bona fide reviews, and the list of contributors to the volume was expanded to include some workers not at the original meeting. The reviewe represent work of high quality, in basic system ranging from “identified neurons” of simple invertebrates to the somatosensory cortex of primates. Topice include the regulation of growing axons by substrate and neurotransmitter interactions, plasticity of central and peripheral synepeee, and analysis of likely candidatea for the cellular mechanism of learning. The entries are well organized and well written, and the production standarda are quite high. The book shouldbe of grent interest to practicing neuroscientista studying neural development and learning.

5 citations