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First published online on March 28, 2002.
 Copyright © 2002 by The Physiological Society
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Received December 18, 2001
Accepted after revision February 22, 2002

Short-term synaptic plasticity, simulation of nerve terminal dynamics, and the effects of protein kinase C activation in rat hippocampus

Darrin H. Brager1*, Marco Capogna2, and Scott M. Thompson1

1 Department of Physiology, University of Maryland School of Medicine, 655 W. Baltimore Street, Baltimore, MD 21201, USA
2 MRC Anatomical Neuropharmacology Unit, University Department of Pharmacology, Mansfield Road, Oxford OX1 3TH, UK

* To whom correspondence should be addressed. E-mail: dbrag001{at}umaryland.edu.

Phorbol esters are hypothesised to produce a protein kinase C (PKC)-dependent increase in the probability of transmitter release via two mechanisms: facilitation of vesicle fusion or increases in synaptic vesicle number and replenishment. We used a combination of electrophysiology and computer simulation to distinguish these possibilities. We constructed a stochastic model of the presynaptic contacts between a pair of hippocampal pyramidal cells that used biologically realistic processes and was constrained by electrophysiological data. The model reproduced faithfully several forms of short-term synaptic plasticity, including short-term synaptic depression (STD), and allowed us to manipulate several experimentally inaccessible processes. Simulation of an increase in the size of the readily releasable vesicle pool and the time of vesicle replenishment decreased STD, whereas simulation of a facilitation of vesicle fusion downstream of Ca2+ influx enhanced STD. Because activation of protein kinase C with phorbol ester enhanced STD of EPSCs in rat hippocampal slice cultures, we conclude that an increase in the sensitivity of the release process for Ca2+ underlies the potentiation of neurotransmitter release by PKC.




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