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Caenorhabditis elegans  is as an ideal model system for the study of mechanisms underlying learning and memory. In the present study, we employed  C. elegans  assay system of thermotaxis memory to investigate the possible role of serotonin neurotransmitter in memory control. Our data showed that both mutations of  tph-1 ,  bas-1 , and  cat-4  genes, required for serotonin synthesis, and mutations of  mod-5  gene, encoding a serotonin reuptake transporter, resulted in deficits in thermotaxis memory behavior. Exogenous treatment with serotonin effectively recovered the deficits in thermotaxis memory of  tph-1  and  bas-1  mutants to the level of wild-type N2. Neuron-specific activity assay of TPH-1 suggests that serotonin might regulate the thermotaxis memory behavior by release from the ADF sensory neurons. Ablation of ADF sensory neurons by expressing a cell-death activator gene  egl-1  decreased the thermotaxis memory, whereas activation of ADF neurons by expression of a constitutively active protein kinase C homologue ( pkc-1 ( gf )) increased the thermotaxis memory and rescued the deficits in thermotaxis memory in  tph-1  mutants. Moreover, serotonin released from the ADF sensory neurons might act through the G-protein-coupled serotonin receptors of SER-4 and SER-7 to regulate the thermotaxis memory behavior. Genetic analysis implies that serotonin might further target the insulin signaling pathway to regulate the thermotaxis memory behavior. Thus, our results suggest the possible crucial role of serotonin and ADF sensory neurons in thermotaxis memory control in  C. elegans .

Serotonin Control of Thermotaxis Memory Behavior in Nematode Caenorhabditis elegans