Is serotonin uptake by peripheral tissues sensitive to hypoxia exposure?

Plasma 5-HT homeostasis is maintained through the combined processes of uptake (via the 5-HT transporter SERT, and others), degradation (via monoamine oxidase, MAO), and excretion. Previous studies have shown that inhibiting SERT, which would inhibit 5-HT uptake and degradation, attenuates parts of the cardiovascular hypoxia reflex in Gulf toadfish (Opsanus beta), suggesting that these 5-HT clearance processes may be important during hypoxia exposure. Therefore, the goal of this experiment was to determine the effects of mild hypoxia on 5-HT uptake and degradation in the peripheral tissues of toadfish. We hypothesized that 5-HT uptake and degradation would be upregulated during hypoxia resulting in lower plasma 5-HT, with uptake occurring in the gill, heart, liver, and kidney. Fish were exposed to normoxia (97.6% O2 saturation, 155.6 torr), or 2-min, 40-min or 24 h mild hypoxia (50% O2 saturation, ∼80 torr), injected with radiolabeled [3H]5-HT and blood, urine, bile and tissues taken. Plasma 5-HT levels were reduced by 40% after 40 min of hypoxia exposure and persisted through 24 h. 5-HT uptake by the gill was upregulated following 2 min of hypoxia exposure, and degradation in the gill was upregulated at 40 min and 24 h. Interestingly, there was no change in 5-HT uptake by the heart and degradation in the heart decreased by 58% within 2 min of hypoxia exposure and by 85% at 24 h. These results suggest that 5-HT clearance is upregulated during hypoxia and is likely driven, in part, by mechanisms within the gill and not the heart.

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Is serotonin uptake by peripheral tissues sensitive to hypoxia exposure?

Cited by 2 publications

References 67 publications

Gulf toadfish (Opsanus beta) gill neuroepithelial cells in response to hypoxia exposure

Gulf toadfish (Opsanus beta) gill neuroepithelial cells in response to hypoxia exposure

Mild hypoxia exposure impacts peripheral serotonin uptake and degradation in Gulf toadfish (Opsanus beta)

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