7. Sensitization to water-soluble sodium acetate in the nematode Caenorhabditis elegans

Matsuura, Tetsuya; Oda, Takayuki; Hayashi, Genta; Sugisaki, Daisuke; Ichinose, Mitsuyuki

doi:10.1016/j.cbpb.2007.07.045

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“…In our preliminary studies, we unexpectedly found that C. elegans pre-exposed to sodium acetate in the agar plate, which was obtained by a concentration gradient of sodium acetate, showed an increase in the chemotactic response to sodium acetate in comparison with naive animals (Matsuura et al, 2007b). The results of our preliminary studies were not consistent with those in previous reports (Wen et al, 1997;Saeki at al., 2001), presumably due to differences in the methods used in the conditioning period.…”

Section: Introductioncontrasting

confidence: 96%

“…3). Moreover, pre-exposed lrn-1 mutants, which have a defect in associative learning in regards to water-soluble attractants, showed an enhancement of chemotactic response to sodium acetate (Matsuura et al, 2007b). The chemotactic response to sodium acetate in animals conditioned in the presence of food with sodium acetate was greater than that of animals maintained in the presence of food only (unpublished observation).…”

Section: Discussionmentioning

confidence: 86%

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Enhancement of Chemotactic Response to Sodium Acetate in the NematodeCaenorhabditis elegans

et al. 2010

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In this study, we investigated the chemotactic response of a wild-type (N2) nematode (Caenorhabditis elegans) to a water-soluble attractant, sodium acetate, after pre-exposure to the chemical. The chemotactic response to 1.0 M sodium acetate of the non-exposed control nematodes was lower than that of the nematodes that were pre-exposed to 1.0 M sodium acetate for 90 min (p < 0.05). The increase in the response to sodium acetate was observed up to 6 hr, but not at 12 hr after exposure. To clarify the mechanism of this enhancement of the chemotactic response, several mutants were used. The chemotactic response of pre-exposed tph-1 and bas-1 mutants, whose main defect was serotonin secretion, was enhanced in comparison with that of the control mutants (p < 0.01). However, cat-1 and cat-2 mutants, which are respectively defective in serotonin and dopamine secretion and dopamine secretion only, showed no enhancement of the chemotactic response to sodium acetate, even when pre-exposed to this chemical. When the cat-1 and cat-2 mutants were pre-exposed to sodium acetate and bred in the presence of 40 mM dopamine, these mutants showed enhanced chemotactic response to sodium acetate (p < 0.05). These results suggest that the enhancement of chemotactic response to sodium acetate after pre-exposure to this chemical is modulated by dopaminergic neurotransmission.

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Section: Introductioncontrasting

confidence: 96%

Section: Discussionmentioning

confidence: 86%