Abstract
The complex performance of the brain and the regulatory processes of the peripheral nervous system are highly dependent on the functioning of the ten billion nerve cells, each of which is connected by synapses to an average of approximately ten thousand other nerve cells. Unlike electronic data processing systems, these interconnections are not rigid but adapt in many ways as a function of the data flow through the neural network. In order to understand the way in which the central nervous system works, and also understand this "plasticity," it is essential to know not only the mechanism of signal transmission but also to understand why and how the intensities of these connections change as a function of data flow. It has been known for a long time that a brief increase in the concentration of calcium inside the signal-emitting (presynaptic) nerve ending is the direct initiator of the release of a messenger substance, the neurotransmitter. This induces an electric signal downstream, i.e. in the "postsynaptic" cell. Transmitter release is a neural specialization of a very general process in cell biology causing signal substances and active substances to be released from a variety of cell types in many sites in the body. Only recently, the majority of the proteins involved have become known, and some first structural data have been elaborated about a macromolecular complex initiating the release reaction.
As far as "plasticity" of the synaptic connection intensity is concerned, especially the phenomenon called long-term potentiation (LTP) has met with particular attention in recent years, as it is believed to play an important role in storing memory contents. Whether long-term potentiation is based on pre- or postsynaptic changes is the subject of controversial discussions. The phenomena of synaptic short-term plasticity have received less attention. Depending on the type of synapse, repetitive excitation at intervals of 0.01 to 0.1 seconds gives rise to facilitation (i.e. an increase in postsynaptic response in the second and all following responses) or the opposite, i.e. a decrease (depression). These changes certainly are no less interesting than LTP, as most actions of the central nervous system are produced over very short time spans, and fast adaptation of the data transmission processes is bound to play an important role in these processes. Facilitation and depression have been described as mainly presynaptic changes, i.e. as increases in or decreases of transmitter releases, already in early studies by Bernhard Katz. Numerous studies in the fifties and sixties have recognized the depletion of a pool of releasable vesicles as the reason for depression. Also, the calcium "residue" remaining in a nerve ending after a first excitation was attributed an effect promoting facilitation when this calcium was superimposed upon the calcium entering during another excitation (the direct initiator of release).
As far as "plasticity" of the synaptic connection intensity is concerned, especially the phenomenon called long-term potentiation (LTP) has met with particular attention in recent years, as it is believed to play an important role in storing memory contents. Whether long-term potentiation is based on pre- or postsynaptic changes is the subject of controversial discussions. The phenomena of synaptic short-term plasticity have received less attention. Depending on the type of synapse, repetitive excitation at intervals of 0.01 to 0.1 seconds gives rise to facilitation (i.e. an increase in postsynaptic response in the second and all following responses) or the opposite, i.e. a decrease (depression). These changes certainly are no less interesting than LTP, as most actions of the central nervous system are produced over very short time spans, and fast adaptation of the data transmission processes is bound to play an important role in these processes. Facilitation and depression have been described as mainly presynaptic changes, i.e. as increases in or decreases of transmitter releases, already in early studies by Bernhard Katz. Numerous studies in the fifties and sixties have recognized the depletion of a pool of releasable vesicles as the reason for depression. Also, the calcium "residue" remaining in a nerve ending after a first excitation was attributed an effect promoting facilitation when this calcium was superimposed upon the calcium entering during another excitation (the direct initiator of release).