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Serotonin control of thermotaxis memory behavior in nematode Caenorhabditis elegans.

Li Y, Zhao Y, Huang X, Lin X, Guo Y, Wang D, Li C, Wang D - PLoS ONE (2013)

Bottom Line: Caenorhabditis elegans is as an ideal model system for the study of mechanisms underlying learning and memory.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.Genetic analysis implies that serotonin might further target the insulin signaling pathway to regulate the thermotaxis memory behavior.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Medical School of Southeast University, Nanjing, China.

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.

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Thermotaxis memory behavior in mod-5 mutants.(A) Extinction of the association (food at 20°C) of wild-type and mod-5(n822) mutant animals. The normalized isothermal tracking behavior (IT) values were used. (B) Comparison of the extinctions of wild-type and mod-5(n822) mutant animals at the time interval of 18-hr. (C) Thermotaxis behavior of wild-type and mod-5(n822) mutant animals. In the thermotaxis assay system, movement to 25°C was scored as thermophilic (T); movement to 17°C was scored as cryophilic (C); movement across the thermal gradient (17°C/25°C) was scored as athermotactic (A); and movement at 20°C was scored as IT. Bars represent means ± S.E.M. **p<0.01.
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pone-0077779-g004: Thermotaxis memory behavior in mod-5 mutants.(A) Extinction of the association (food at 20°C) of wild-type and mod-5(n822) mutant animals. The normalized isothermal tracking behavior (IT) values were used. (B) Comparison of the extinctions of wild-type and mod-5(n822) mutant animals at the time interval of 18-hr. (C) Thermotaxis behavior of wild-type and mod-5(n822) mutant animals. In the thermotaxis assay system, movement to 25°C was scored as thermophilic (T); movement to 17°C was scored as cryophilic (C); movement across the thermal gradient (17°C/25°C) was scored as athermotactic (A); and movement at 20°C was scored as IT. Bars represent means ± S.E.M. **p<0.01.

Mentions: Moreover, we found that mutations of mod-5 gene, encoding a serotonin reuptake transporter, also significantly decreased the thermotaxis memory compared with wild-type N2 (Fig. 4A). mod-5(n822) mutants exhibited the decreased half maximal extinction and percentages of animals performing IT at the time interval of 18-hr (Figs. 4A and 4B). mod-5(n822) mutants showed the normal thermotaxis behavior like wild-type N2 (Fig. 4C).


Serotonin control of thermotaxis memory behavior in nematode Caenorhabditis elegans.

Li Y, Zhao Y, Huang X, Lin X, Guo Y, Wang D, Li C, Wang D - PLoS ONE (2013)

Thermotaxis memory behavior in mod-5 mutants.(A) Extinction of the association (food at 20°C) of wild-type and mod-5(n822) mutant animals. The normalized isothermal tracking behavior (IT) values were used. (B) Comparison of the extinctions of wild-type and mod-5(n822) mutant animals at the time interval of 18-hr. (C) Thermotaxis behavior of wild-type and mod-5(n822) mutant animals. In the thermotaxis assay system, movement to 25°C was scored as thermophilic (T); movement to 17°C was scored as cryophilic (C); movement across the thermal gradient (17°C/25°C) was scored as athermotactic (A); and movement at 20°C was scored as IT. Bars represent means ± S.E.M. **p<0.01.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3815336&req=5

pone-0077779-g004: Thermotaxis memory behavior in mod-5 mutants.(A) Extinction of the association (food at 20°C) of wild-type and mod-5(n822) mutant animals. The normalized isothermal tracking behavior (IT) values were used. (B) Comparison of the extinctions of wild-type and mod-5(n822) mutant animals at the time interval of 18-hr. (C) Thermotaxis behavior of wild-type and mod-5(n822) mutant animals. In the thermotaxis assay system, movement to 25°C was scored as thermophilic (T); movement to 17°C was scored as cryophilic (C); movement across the thermal gradient (17°C/25°C) was scored as athermotactic (A); and movement at 20°C was scored as IT. Bars represent means ± S.E.M. **p<0.01.
Mentions: Moreover, we found that mutations of mod-5 gene, encoding a serotonin reuptake transporter, also significantly decreased the thermotaxis memory compared with wild-type N2 (Fig. 4A). mod-5(n822) mutants exhibited the decreased half maximal extinction and percentages of animals performing IT at the time interval of 18-hr (Figs. 4A and 4B). mod-5(n822) mutants showed the normal thermotaxis behavior like wild-type N2 (Fig. 4C).

Bottom Line: Caenorhabditis elegans is as an ideal model system for the study of mechanisms underlying learning and memory.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.Genetic analysis implies that serotonin might further target the insulin signaling pathway to regulate the thermotaxis memory behavior.

View Article: PubMed Central - PubMed

Affiliation: Key Laboratory of Developmental Genes and Human Disease in Ministry of Education, Medical School of Southeast University, Nanjing, China.

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.

Show MeSH