A Model of the Possible Role of Gaseous Neuromessenger Nitric Oxide in Synaptic Potentiation

Abstract

The experimental studies show that NO can both enhance glutamate release from the presynapse and inhibit Ca⁺⁺ influx in the postsynapse. In this paper, a theoretical model is presented to study these roles of NO in synaptic potentiation. In the model, NO is assumed to be produced in the postsynapse and diffuse into the extracellular space and then to the presynapse. Two kinds of excitatory receptor channels, NMDA and non-NMDA channels, are considered in the postsynaptic membrane. NO mediated glutamate release in the presynapse is expressed as the increase of the open channels in the postsynapse, and NO also decreases NMDA current since NMDA channel modulates Ca⁺⁺ influx. Our simulations show that at low concentration of NO (0.5 uM), NO depresses the synaptic potentiation when a tetanus stimulation is delivered, but at high concentration ( l0uM), NO facilitates the synaptic potentiation. The membrane permeability, and the diffusion coefficient of NO are significant factors in determining the integrated function of NO in synaptic potentiation because they determine the concentration difference between the pre-and postsynaptic cells. Although accurate experimental measurements of all these parameters are not available, the model presented predicts that only at relatively high NO concentration levels, does NO facilitate production of LTP.