Abstract
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.
Highlights
Memory can be defined as encoding, storage and retrieval of learning inputs in human and animals [1]
To ensure that the altered thermotaxis memory behaviors in tph-1, bas-1, and cat-4 mutants were not due to the deficits in thermotaxis behavior, we examined the thermotaxis behaviors in tph-1(mg280), bas-1(ad446), and cat4(e1141) mutants
These data demonstrate that genes required for serotonin synthesis are essential for thermotaxis memory control in C. elegans
Summary
Memory can be defined as encoding, storage and retrieval of learning inputs in human and animals [1]. Nematode Caenorhabditis elegans is an excellent model organism to study the biological processes relevant to a wide variety of human behavior and the related disease systems [2]. In 1990, the C. elegans was suggested as an ideal model system for study of the mechanisms underlying learning and memory [3]. The worms have a simple nervous system comprising 302 neurons which are all well identified, and the connectivity between all neurons has been fully mapped [4,5]. Many components such as neurotransmitters and their respective receptors in the nervous system of C. elegans are similar to those in mammals [4]. C. elegans displays several forms of memory, such as memory to thermotaxis, chemotaxis, and mechanotransduction [1]
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