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GENERAL MODEL FOR THE MOLECULAR EVENTS IN SYNAPSES DURING LEARNING MATTI O. HUTTUNEN* Any biochemical theory about the synaptic events during learning should be based on the assumption that the critical physiological phenomenon in learning is the very first activation of a previously nonfunctional synapse. Once the nonfunctional synapse has become usable, the essential event that is responsible for learning has taken place [I]. Unfortunately, most of the presented biochemical theories about learning do not propose anything about this basic physiological phenomenon in learning but are content to suggest vaguely "specific" changes in the neuronal metabolism of proteins, nucleic acids, etc. At the same time, it seems to be the opinion of many critical neurobiologists that our present state of knowledge about the neuronal metabolism is too scattered to permit the formulation of any detailed theory about the molecular events in synapses during learning. It is, however, a fact that our inability to measure directly these extremely fast chemical reactions compels us to approach the biology of learning intuitively—from a detailed theory to experiments. In this communication an effort has been made to formulate a general model for the chemical events in the activation of a previously nonfunctional synapse. The purpose of the author is not to claim this model to be ultimately the right one, but rather to show that in spite of our diversified knowledge it is possible to present a realistic detailed chemical model for this essential event in memory fixation. The present theory is a modification of a hypothesis presented previously by the author [2, 3]. The majority of the synapses in the central nervous system are probably congenitally functional [4]. This genetically determined network of neurons is the backbone of any learning, as "learning" always involves the coupling of an unconditional stimulus with a conditional stimulus [I]. Learning and memory, however, would not be possible in any form without the existence of a particular group of nonfunctional synapses which "open" only as the result of a specific unconditional stimulus from * Department of Medical Chemistry, University of Helsinki, Siltavuorenpenger 10 A, SF-00170 Helsinki 17, Finland. Perspectives in Biology and Medicine · Autumn 1973 | 103 the environment. Moreover, it has been shown that memory fixation is dependent on the emotional arousal of the nervous system [5]. It is probable that the arousal state of the neurons is regulated through the special congenitally determined neuronal connections. Recently it has been proposed that the arousal state of an individual neuron is regulated through the special network of neurons that use catecholamines as their transmitters [6]. The above-described physiological conditions for "learning" at the level of an individual neuron are schematically presented in figure 1. In this figure three presynaptic neurons A, B, and C have a synaptic connection with a postsynaptic neuron X. The synapse B -^ X is supposed to be a nonfunctional "learning" synapse. It is only after "learning" that this synapse ¿? —» X becomes able to transfer neuronal stimuli from the neuron B to the neuron X. On the other hand, the synapses A -^ X and C -» X are supposed to be congenitally functional synapses. The neuron A is assumed to bring unconditional sensory stimuli to the neuron X, whereas the neuron C is supposed to regulate the arousal state of the neuron X. In the following chemical model of learning, the neuron C is presumed to use norepinephrine as its chemical transmitter. Now, the basic physiological condition for the "opening" of a previously nonfunctional synapse was the coupling of an unconditional sensory stimulus (A) with a conditional stimulus (B) during the aroused neuronal state. With the symbols of our figure, the "opening" of the synapse £ —» X can occur only when the neuron X is depolarized during the simultaneous firing of all three presynaptic neurons A, B, and C. What, then, are the molecular events in the synapse B -» X resulting in its transformation from a nonfunctional to a functional state? It has been suggested that the most plausible cause for the extremely fast phenomenon of memory fixation is a sudden modification of the response of the postsynaptic membrane to a chemical transmitter [7]. In our model, we assume that the nonfunctional state of the synapse...

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Additional Information

ISSN
1529-8795
Print ISSN
0031-5982
Pages
pp. 103-108
Launched on MUSE
2015-01-07
Open Access
No
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