Octopamine affects neurotransmitter release in crayfish neuromuscular junction through residual calcium

Abstract

Octopamine and serotonin produce opposite responses in both crayfish behavior and in the crayfish neuromuscular junction. With this correlation in mind, we sought to discover whether octopamine and serotonin shared a pathway responsible for facilitating neurotransmitter release. We explored a specific aspect of this pathway, namely the effect of residual calcium on EPSP amplitudes in the crayfish superficial extensor neuromuscular junction. Calcium plays an important role in signal transmission, and there are several ways in which it can do so. Residual calcium facilitates transmission by prompting the release of more synaptic vesicles through exocytosis into the synaptic gap. Research has shown that serotonin does not use residual calcium to facilitate synaptic transmission in crayfish muscle cells, so we hypothesized that octopamine would not either. In order to test this, we stimulated the second ganglionic nerve with a paired set of two electrical pulses in quick succession, and measured the amplitudes of the EPSPs they produced, both with and without octopamine. We then measured the percent change from the first to the second EPSP to quantify the effect of residual calcium on signal transmission, as excess calcium ions remain in the presynaptic cell between pulses. We found that, contrary to our hypothesis, octopamine does affect the amount of residual calcium in the cell. In fact, there is a significant decrease in facilitation by residual calcium in the presence of octopamine.