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Effects of Thalidomide on the Serotonergic Neurogenesis of Sea Urchin Embryos

Thalidomide, an anti-nausea drug, produces teratogenic effects in human embryos. Sea urchin species initially develop similarly to human embryos, making them viable models to study developmental effects. Previous research indicates that sea urchin embryos are sensitive to thalidomide induced malformations and showed phenotypic defects. Sea urchins possess a simple nerve network containing serotonergic neurons, which thalidomide may alter during development. Sea urchin gametes were studied in seawater, dimethyl sulfoxide (DMSO), and thalidomide concentration cultures. Embryo malformations were recorded at 24, 48, and 72 hours. Primary goat anti-rabbit serotonin antibody with secondary Vectafluor DyLight horse anti-goat antibody added was used to stain for serotonin, while NucBlue DAPI staining was used for cell counts. Preliminary results show that thalidomide exposure results in significantly more malformations than controlled cultures. Thalidomide exposed embryos may have fewer neurons binding to serotonin. Findings could provide insight into the mechanism of thalidomide-induced peripheral neuropathy in humans.