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1 Johannes Mueller Institute of Physiology, Humboldt University, Berlin, Germany; Institute of Theoretical Biology, Humboldt University, Berlin, Germany
2 Institute of Theoretical Biology, Humboldt University, Berlin, Germany
3 Institute of Physiology, University of Freiburg, Freiburg, Germany
4 Institute of Physiology and Pathophysiology, Ruprecht-Karls University, Heidelberg, Germany
* To whom correspondence should be addressed. E-mail: r.ritz{at}biologie.hu-berlin.de.
The nervous system adapts to experience by changes in synaptic strength. The mechanisms of synaptic plasticity include changes in the probability of transmitter release and in postsynaptic responsiveness. Experimental and neuro-pharmacological evidence points towards a third variable in synaptic efficacy, namely changes in presynaptic transmitter concentration. Several groups, including our own, have reported changes in the amplitude and frequency of postsynaptic (miniature) events indicating that alterations in transmitter content cause alterations in vesicular transmitter content and vesicle dynamics. It is, however, not a priori clear how transmitter metabolism will affect vesicular transmitter content and how this, in turn, will affect pre- and postsynaptic functions. We therefore have constructed a model of the presynaptic terminal incorporating vesicular transmitter loading and the presynaptic vesicle cycle. We hypothesize that the experimentally observed synaptic plasticity following changes in transmitter metabolism puts predictable restrictions on vesicle loading, cytoplasmic-vesicular transmitter concentration gradient, and on vesicular cycling or -release. The results of our model depend on the specific mechanism linking presynaptic transmitter concentration to vesicular dynamics, i.e. alteration of vesicle maturation or alteration of release. It does also make a difference whether differentially filled vesicles are detected and differentially processed within the terminal or whether vesicle filling acts back onto the terminal via presynaptic autoreceptors. Therefore, the model allows one to decide, at a given synapse, how transmitter metabolism is linked to presynaptic function and -efficacy.
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