Neuronal degeneration and reorganization: a mutual principle in pathological and in healthy interactions of limbic and p
Based on developmental principles and insights from animal research about neuroplasticity in cell assemblies, this article is to propose a view of plasticity that promotes a link between hippocampal and prefrontal structure and function. Both the mitotic
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Summary. Based on developmental principles and insights from animal research about neuroplasticity in cell assemblies, this article is to propose a view of plasticity that promotes a link between hippocampal and prefrontal structure and function. Both the mitotic activity (counting of BrdU-Iabeled cells) in hippocampal dentatus and the maturation of dopamine fibres (quantitative immunochemistry of mesoprefrontal projection) in the prefrontal cortex proved to be a measurable combination for investigating the complex chain of events that relate activity dependent neuroplasticity to normal as well as to pathological maturational processes. With our animal model we demonstrate that both rearing conditions and neuroactive substances can effectively interfere with developmental plasticity and induce a malfunctional adaptation of prefrontal structures and neurotransmitter systems (dopamine, GABA). In the hippocampal dentatus, where ontogenetic plasticity proved to be preserved by continued neuro- and synaptogenesis, serious damage can be internalized without simultaneous disruption of neural dynamics offering an approach to reverse dysfunctional reorganization in the prefrontal cortex.
Introduction
This article is to draw attention to the fact that degeneration is a prerequisite for neuroplastic reorganization not only in pathological but also in healthy interactions of higher brain systems . Years of tedious experimental work has been required to shed light on this new way of looking at the phenomenon of natural neuroplasticity under the influence of regressive events. The main historical steps which led from Hebb, who was the pioneer in the field of neuroplasticity, to Wolff are indicated in Fig. 1. Hebb (1949) offered a concept of reverberatory activity based on the idea, that if sensory stimuli repeatedly or persistently activate single neurons in an assembly (cells against the background arrow in Fig. 1A), the arrangement of connections is set according to the activity flow, and metabolic changes increase the efficiency of connections, thereby, stabilizing the assembly . This
P. Riederer et al. (eds.), Advances in Research on Neurodegeneration © Springer-Verlag Wien 2000
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G. Teuchert-Noodt
A
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Hebbs concept of reverberatory activity in a cell assembly.
B
Lesion induced reactive genesis in the brain.
synapto-
Wolff's concept of compensatory synaptogenesis in ontogenesis.
Fig. lA-Co Schemes depicting the main historical stages of neuroplasticity research from Hebb (1949) to Wolff (1983). Hebb's cell assembly is an adequate model to illustrate the reactive plasticity as it is induced by injury (black bar indicating cut in B) and the compensatory synaptogenesis as it is induced by morphogens (C). The two hazy areas near the dark neurons indicate synapse remodeling
bioelectrically induced structural and functional adaptation could empirically be affirmed by the detection of longterm potentiation (LTP) and neuroplastic metabolites, as generated by enhanced NMDA-synaptic currents (see Kandel et aI., 19
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