Abstract
The selective serotonin reuptake inhibitor (SSRI) fluoxetine (FLX), the active ingredient of the antidepressant drug Prozac, inhibits reuptake of the neurotransmitter, serotonin (5-HT; 5-hydroxytryptamine), into cells by the 5-HT transporter (SERT). Given the role of 5-HT in oxygen detection and the cardiovascular and ventilatory responses of fish to hypoxia, we hypothesized that treatment of the Gulf toadfish, Opsanus beta, with FLX would interfere with their response to hypoxia. Toadfish treated intra-arterially with 3.4 μg.g−1 FLX under normoxic conditions displayed a transient tachycardia and a biphasic caudal arterial blood pressure (PCA) response that are in direct conflict with the typical hypoxia response. Fish injected intraperitoneally with FLX under normoxia had resting cardiovascular and ventilatory parameters similar to controls. Upon exposure to hypoxia, control toadfish exhibit a significant bradycardia, reduction in PCA and an increase in ventilatory amplitude (VAMP) without any changes in ventilatory frequency (fV). Fish treated IP with 10 μg.g−1 FLX showed an interference in the cardiovascular and ventilatory response to hypoxia. Interestingly, when treated with 25 μg.g−1 FLX, the bradycardia and VAMP response to hypoxia were similar to control fish while the PCA response to hypoxia was further inhibited. These results suggest that SERT inhibition by FLX may hinder survival in hypoxia.
Highlights
Synthesis of 5-HT de novo from endogenous tryptophan[22]
Teleost fish react with a suite of cardiovascular and ventilatory responses: a decrease in heart rate or bradycardia, a change in systemic and/or branchial vascular resistance resulting in changes in blood pressure, and an increase in ventilation amplitude (VAMP) and/or ventilation frequency, all responses aimed to optimize O2 exchange across the gill and maintain metabolic rate[24,25,26,27,28,29,30,31,32,33,34,35]
During the pre-injection period, there were no significant differences measured between the heart beat frequency, pulse pressure (PP; mmHg), which was used as an indicator of heart stroke volume, caudal arterial blood pressure (PCA; mmHg), ventilation amplitude (VAMP; mmHg), and ventilation frequency of saline- and FLX-injected fish (Table 1)
Summary
Synthesis of 5-HT de novo from endogenous tryptophan[22]. Interestingly, isolated perfused trout gills have been shown to extract 80% of the 5-HT from the perfusate[23], which could indicate a high capacity for 5-HT reuptake. We hypothesize that FLX treatment may attenuate or abolish the cardiovascular and/or ventilatory response to hypoxia, either by disrupting O2 sensing by fish NECs or by stimulating or desensitizing peripheral 5-HT receptors that mediate cardiovascular and ventilatory changes as a consequence of increased circulating 5-HT. To test this hypothesis, Gulf toadfish, Opsanus beta, were first injected IA with FLX to determine the cardiovascular and ventilatory effects of FLX alone. Toadfish were treated intraperitoneally (IP) with FLX and exposed to hypoxia to determine whether FLX treatment interfered with the cardiovascular and ventilatory response to hypoxia
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