DSTs may affect the swimming ability of marine medaka by interfering with the neurotransmitter system and calcium signaling
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Updated: Jun 12, 2026

Swimming Induced Paralysis to Assess Dopamine Signaling in Caenorhabditis elegans
Published on: April 3, 2019
Zi-Min Chen1, Mei-Qi Li1, Jing-Xuan Jiang1
1College of Life Science and Technology, Key Laboratory of Aquatic Eutrophication and Control of Harmful Algal Blooms of Guangdong Higher Education Institute, Jinan University, Guangzhou, 510632, China.
Abstract:
Diarrhetic shellfish toxins (DSTs) are the most widely distributed algal toxins in marine environment. Although DSTs exhibit diverse toxic effects, their neurotoxicity on marine fish remains poorly understood. Swimming behavior of fish is a sensitive indicator of neurotoxicity, and locomotor ability is of vital importance for their survival. This study systematically investigated the impact of exposure to the DSTs-producing dinoflagellate Prorocentrum lima (2 × 106 cells/L) on swimming behavior in the marine model fish Oryzias melastigma and explored potential neurotoxicity-related mechanisms. After 96 h of exposure, the fish showed significant reductions in average swimming speed, acceleration, and total distance, along with increased frozen events and altered swimming trajectories. Correspondingly, brain tissue damage was observed, accompanied by marked decreases in neurotransmitter levels, including acetylcholine, dopamine, and serotonin. Transcriptomic analysis suggested potential disturbances in neurotransmitter system, calcium signaling, and myelination following DSTs exposure. The altered expressions of irak4, il-1b, il-12, atr, sesn1, and ppm1d pointed to the activation of oxidative stress and inflammatory responses, which likely exacerbate neural damage. This structural compromise was further supported by the inhibition of ECM-receptor interaction and focal adhesion pathway. Crucially, detected brain DSTs and molecular docking suggested that Slco1d1 may be involved in DSTs-associated brain toxicity, although its role in mediating DSTs across the blood-brain barrier remains to be verified. Collectively, these findings indicate that DSTs-producing algal exposure may impair swimming behavior and neural function in marine medaka, potentially involving neurotransmitter dysregulation, calcium signaling disturbance, myelination-related changes, and brain tissue injury.
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