Skip to main content
. 2001 Aug 15;21(16):5871–5884. doi: 10.1523/JNEUROSCI.21-16-05871.2001

Fig. 8.

Fig. 8.

Models for the effects of fluoxetine on C. elegans behaviors. A, MOD-5 CeSERT acts upstream of the MOD-1 5-HT-gated chloride channel and the GOA-1 G-protein.B, The potentiating effect of low concentrations of fluoxetine on the enhanced slowing response is 5-HT- and MOD-5 CeSERT-dependent. The stimulus of food in a food-deprived animal results in the release of 5-HT. This 5-HT acts through the MOD-1 5-HT-gated chloride channel and through a GOA-1-dependent 5-HT signaling pathway, which likely acts in parallel to the MOD-1 pathway. Together, these two pathways result in the slowing of the locomotory rate. Mutation in mod-5 or application of fluoxetine leads to inefficient clearing of 5-HT and thus a hyperenhanced slowing response. 5-HT receptor, A metabotropic 5-HT receptor that GOA-1 might couple to. Triangles, 5-HT;circles, chloride ions. C, The effects of high concentrations of fluoxetine on egg laying, nose contraction, and paralysis are MOD-5 CeSERT-independent. High concentrations of fluoxetine act on non-SERT targets and on a non-5-HT pathway to paralyze C. elegans and to lead to the contraction of nose muscles. By contrast, stimulation of egg laying by fluoxetine is MOD-5 CeSERT-independent but still partially dependent on 5-HT (for details, see Discussion).