Showing papers on "Developmental plasticity published in 1988"

Post-Lesion Neural Plasticity

Abstract: Neural networks are not rigidly wired but rather highly plastic structures, the functional architecture of which can be actively reorganized in response to external or internal events. Lesions of such networks induce plastic processes which in time may lead to a recovery of the initially disrupted function. This type of neural plasticity is the main focus of the book, which presents a broad spectrum of experimental paradigms for lesion-induced plasticity as in the spinal cord, the vestibular, oculomotor, visual and olfactory system, the cerebellum and the cerebral cortex, including recent methodological developments. Concepts and perspectives in understanding neural plasticity are reported in reviews and original research reports and are thoroughly discussed.

Cytoarchitectonic parameters of developmental capacity of the human associative auditory cortex during postnatal life.

Abstract: In order to determine the developmental capacity of the human auditory cortex we studied the 'regressive' cytoarchitectonic events during perinatal and postnatal development: disappearance of fetal elements and cytoarchitectonic reorganization. Studies were done on Nissl-stained serial sections of human temporal cortex in the specimens ranging from 24 weeks of gestation to the 3rd postnatal year. The fetal layers were regularly found in the newborn in the posterior associative auditory cortex. The fetal subplate zone disappeared gradually over the first 3 postnatal months, indicating decline in the growth of the major cortical fibre systems. The fetal types of neurons have been found however also in older specimens in the associative auditory cortex. The auditory cortex also contains in the postnatal period some fetal elements which indicate the presence of prolonged anatomical developmental plasticity.

Quantitative morphology of synaptic plasticity in the aging brain.

Abstract: Quantitation of synaptic ultrastructural changes is of great importance in neurobiology, since merely qualitative alterations, if not extreme, are not readily detectable. In the present paper we discuss our previous and present findings on the number (numerical density: Nv), size (average length of the synaptic profiles: L) and surface contact area (surface density: Sv) of the synaptic junctions in aging rodent and human brains. We found that number and size of the synapses are in a close inverse relationship so as to maintain the total surface contact are among the nerve cells constant. These three parameters are closely related to each other, their quantitation may thus represent a reliable index of the morphological aspects of synaptic plasticity, i.e. the modification of ultrastructure occurring at synaptic membranes after transient changes in synaptic activity. During aging, the morphological plasticity of synapses appears to be seriously impaired: the number of synapses and the total surface contact area among the nerve cells are markedly reduced. However, old nerve cells seem to retain the ability to modify their synaptic endings and to partially compensate for the reduced surface density of the contact zones by expanding the average size of the persisting junctions. Our recent studies on synaptic plasticity in human brains from old and demented subjects showed that while the size of the synaptic contacts remains constant, the numerical and surface densities undergo a further decrease in demented brains relative to that in normal aging.

Effect of target and non-target transplants on neuronal survival and axonal elongation after injury to the developing spinal cord.

Abstract: Publisher Summary This chapter determines: (1) whether transplants of fetal spinal cord tissue at the lesion site can prolong the critical period for developmental plasticity of the corticospinal system, and (2) whether the requirements for survival of immature axotomized neurons are target specific, or whether a variety of immature tissues can substitute for the normal target and support these neurons after injury. Target-specific transplants extend the critical period for developmental plasticity of the corticospinal pathway beyond that seen after lesions alone are demonstrated in the chapter. The corticospinal (CS) axons damaged prior to synaptogenesis are found to exhibit a greater degree of growth than those injured after synaptogenesis is completed, suggesting that an interaction of environmental and neuronal factors regulate the capacity of immature corticospinal neurons for growth. Many immature CNS neurons undergo massive retrograde cell loss in response to target removal by axotomy. At acute survival times, both target and non-target transplants are able to support the temporary survival of axotomized red nucleus (RN) neurons, perhaps by providing a diffusable trophic support for the injured neurons. However, their permanent survival is supported only by target-specific transplants, and they may require axonal elongation and synaptogenesis.

Visual System Development, Plasticity

Abstract: In research on visual system development, as eisewhere, the concept of plasticity has meant different things to different people at different times, and it is unlikely that the evolution of the meaning of the term is over. Any attempt at definition must thus take into account the plasticity of “plasticity.” In speaking broadly of 20th Century neurobiology, it is useful to distinguish three roughly successive periods. During the earliest phase, a major concern of investigators was with the issue of whether the adaptive Organization of the visual system reflects predesign based on genetic information, as opposed to processes of adaptive shaping based on functional effectiveness. Plasticity was used to characterize the latter alternative and was understood to mean “the capacity to adjust functional Organization based on sensory experience.” In subsequent years, attention shifted to documenting the existence of orderly patterns of anatomical connections in the visual pathways and to the hypothesis that these resulted from a refined capacity of outgrowing axons to recognize and distinguish between target neurons based on cytochemical affinities. During this period, plasticity became more specifically linked to problems of anatomical Connectivity but largely lost its reference to the broader problem of accounting for functionally appropriate Organization. The term was generally used to refer to any phenomenon suggesting a capacity to make a pattern of connections other than the “normal” one, hence challenging the chemoaffinity hypothesis.

Protein Kinase C and Protein F1: Potential Molecular Mediators of Lesion-Induced Synaptic Plasticity Recapitulate Developmental Plasticity

Abstract: This review is focused on the suggestion that a potential molecular mechanism involving protein kinase C and its substrate protein F1 may be directly involved in the process of mediating lesion-induced neuronal plasticity. As several chapters in this Volume illustrate, after damage to the nervous system, intact neurons show growth activities such as axonal sprouting. Under certain conditions this can lead to recovery of function, in whole or in part. The mechanisms for this process are not known, though some recent clues from biochemistry suggest particular proteins that may be essential for the process. In this review I wish to emphasize one essential point: that the input-dependent molecular mechanism related to synaptic growth of intact synapses is also recruited by injury-produced growth factors that stimulate the response to nerve injury.