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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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Effects of exogenous serotonin and dopamine on thermotaxis memory behavior in tph-1 or bas-1 mutants.(A–B) Effects of exogenous serotonin on thermotaxis memory behavior in tph-1 mutants. (C–D) Effects of exogenous serotonin on thermotaxis memory behavior in bas-1 mutants. (E–F) Effects of exogenous dopamine on thermotaxis memory behavior in bas-1 mutants. Serotonin or dopamine was dissolved in M9 buffer and spread on the NGM plates at a final concentration of 2 mM or 5 mM. The normalized isothermal tracking behavior (IT) values were used. 5-HT, serotonin; DA, dopamine. Bars represent means ± S.E.M. *p<0.05, **p<0.01. NS, no significance.
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pone-0077779-g002: Effects of exogenous serotonin and dopamine on thermotaxis memory behavior in tph-1 or bas-1 mutants.(A–B) Effects of exogenous serotonin on thermotaxis memory behavior in tph-1 mutants. (C–D) Effects of exogenous serotonin on thermotaxis memory behavior in bas-1 mutants. (E–F) Effects of exogenous dopamine on thermotaxis memory behavior in bas-1 mutants. Serotonin or dopamine was dissolved in M9 buffer and spread on the NGM plates at a final concentration of 2 mM or 5 mM. The normalized isothermal tracking behavior (IT) values were used. 5-HT, serotonin; DA, dopamine. Bars represent means ± S.E.M. *p<0.05, **p<0.01. NS, no significance.

Mentions: To further investigate the role of serotonin in thermotaxis memory control, we examined the effects of exogenous treatment with 2 mM of serotonin on thermotaxis memory behavior in tph-1 and bas-1 mutants. Exogenous treatment with 2 mM of serotonin effectively recovered the deficits in thermotaxis memory of tph-1(mg280) and bas-1(ad446) mutants to the level of wild-type N2 (Figs. 2A–2D). Serotonin treated tph-1(mg280) and bas-1(ad446) mutants exhibited the similar half maximal extinction and percentages of animals performing IT at the time interval of 18-hr to those of wild-type N2 (Figs. 2A–2D).


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)

Effects of exogenous serotonin and dopamine on thermotaxis memory behavior in tph-1 or bas-1 mutants.(A–B) Effects of exogenous serotonin on thermotaxis memory behavior in tph-1 mutants. (C–D) Effects of exogenous serotonin on thermotaxis memory behavior in bas-1 mutants. (E–F) Effects of exogenous dopamine on thermotaxis memory behavior in bas-1 mutants. Serotonin or dopamine was dissolved in M9 buffer and spread on the NGM plates at a final concentration of 2 mM or 5 mM. The normalized isothermal tracking behavior (IT) values were used. 5-HT, serotonin; DA, dopamine. Bars represent means ± S.E.M. *p<0.05, **p<0.01. NS, no significance.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0077779-g002: Effects of exogenous serotonin and dopamine on thermotaxis memory behavior in tph-1 or bas-1 mutants.(A–B) Effects of exogenous serotonin on thermotaxis memory behavior in tph-1 mutants. (C–D) Effects of exogenous serotonin on thermotaxis memory behavior in bas-1 mutants. (E–F) Effects of exogenous dopamine on thermotaxis memory behavior in bas-1 mutants. Serotonin or dopamine was dissolved in M9 buffer and spread on the NGM plates at a final concentration of 2 mM or 5 mM. The normalized isothermal tracking behavior (IT) values were used. 5-HT, serotonin; DA, dopamine. Bars represent means ± S.E.M. *p<0.05, **p<0.01. NS, no significance.
Mentions: To further investigate the role of serotonin in thermotaxis memory control, we examined the effects of exogenous treatment with 2 mM of serotonin on thermotaxis memory behavior in tph-1 and bas-1 mutants. Exogenous treatment with 2 mM of serotonin effectively recovered the deficits in thermotaxis memory of tph-1(mg280) and bas-1(ad446) mutants to the level of wild-type N2 (Figs. 2A–2D). Serotonin treated tph-1(mg280) and bas-1(ad446) mutants exhibited the similar half maximal extinction and percentages of animals performing IT at the time interval of 18-hr to those of wild-type N2 (Figs. 2A–2D).

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