Changes in Synaptic Delay and EPSP Amplitude Induced by TEA with 3,4-DAP, Temperature and Post-Tetanic Potentiation

Abstract

We tested the current model of calcium influx and neurotransmitter release mechanisms by measuring changes in synaptic delay and amplitude of excitatory post-synaptic potentials (EPSPs). Changes in calcium influx and neurotransmitter release were generated following the application of tetraethylammonium bromide (TEA) with 3,4- Diaminopyridine (DAP), post-tetanic potentiation (PTP), and temperature variation at the crayfish neuromuscular junction. Previous research has shown that TEA with 3,4-DAP broadens the pre-synaptic action potential, which increases synaptic delay and EPSP amplitude. PTP, however, has been found to increase the rate of calcium influx, thereby decreasing delay and increasing EPSP amplitude. Other research demonstrated that an increase in temperature narrowed pre-synaptic action potentials, which should decrease delay and decrease EPSP amplitude. We hypothesized that these independent variables would have the predicted effects based on the model for both dependent variables: TEA and decreased temperature would increase delay and EPSP amplitude, while PTP would decrease delay and increase EPSP amplitude. Using intracellular recording, we began and ended each trial under normal conditions to establish a baseline and to test the reversibility of each variable. Our results supported the current model that TEA and temperature would increase synaptic delay, and that TEA and PTP would increase EPSP amplitude. However, we found that a decrease in temperature decreased EPSP amplitude and PTP did not significantly decrease delay, signifying that these variables must affect different mechanisms involved in synaptic transmission.