Serotonin and fluoxetine cause paired pulse depression in typically facilitating synapses in crayfish neuromuscular junction

Abstract

Serotonin, a neurotransmitter in humans, affects synaptic plasticity when used as a modulator with and without the presence of fluoxetine, a serotonin reuptake inhibitor. Most previous research has shown that serotonin causes synaptic facilitation when subjected to long-term stimulation, and experiments on fluoxetine have had mixed results, with some showing facilitation and others showing depression. Our experiment tested the effect of serotonin and serotonin with fluoxetine. We recorded EPSPs after paired pulse stimulation in the crayfish neuromuscular junction while exposed to these chemicals to learn if the chemicals cause paired pulse stimulation or depression in crayfish, which use serotonin as a modulator. Our results showed that serotonin as well as serotonin with fluoxetine caused paired pulse depression in postsynaptic potentials when the control condition yielded paired pulse facilitation. However, the percent change in EPSP amplitude was greater in just serotonin than in serotonin plus fluoxetine. These results indicate that when used as a modulator in the crayfish neuromuscular junction, as opposed to a neurotransmitter, serotonin does not facilitate enhanced synaptic plasticity. Fluoxetine, however, decrease the paired pulse depression caused by serotonin.