Abstract:
Okadaic acid (OA), a naturallt occuring marine toxin, causes diarrhetic shellfish poison (DSP) in human. OA is an inhibitor of protein phosphatase 1A. Previous study showed that OA induced tau hyperphosphorylation, leading to loss of learning and memory. Normally, estrogen has an important role on an enhancement of memory formation. It is probable that OA-induced memory loss may associate with estrogen synthesis in hippocampal neurons. By using H19-7 hippocampal neuron, the effect of concentration and incubation time of OA on cell viability was studied by MTT assay. The synaptic genes expression was study by real-time PCR. The secretion of estrogen was measured by ELISA. The result showed that the incubation of OA at hidh concentration (0.1 and 1 uM) for 24 h significant decreased the viability of cellcompared with be the control. After 48 h treatment, 0.01 uM OA significantly decreased cell viability. The decrease of cell viability is approximately 70% at 78 h and remainstable until 120 h. Moreover, OA treatment decreased the expression of NR2 and PSD-95 genes at 24 and 92 h, respectively. Finally, treatment of OA tented to decrease the estrogen secretion but was not statistically significant. The present study concluded that OA decreased synaptic gene expression, which may cause of memory loss.