Figure 3: 5-HT and the SER-5 receptor transduce ASI inhibition of ASHs.

(a) ASH calcium responses to 10 mM CuSO₄ in wild-type, ASI neurotransmission blocked, ser-5 mutant, and ser-5p::ser-5 and ASH::ser-5 genetically rescued worms. Summation of the kinematics of Cu²⁺ avoidance behaviours (b,c) and Cu²⁺ sensitivity (d, n≥8 assays) in the worms mentioned above. (e) The expression pattern of ser-5p::ser-5::sl2-GFP and sra-6p::R-GECO1 in ser-5-null mutants. These genes were co-expressed in ASH neurons. Scale bar, 20 μm. (f) The tph-1 lof mutation had a similar effect on the ASH Cu²⁺-elicited Ca²⁺ signals as did genetically silencing ASI with TeTx, and the defect was rescued by tph-1p::tph-1 ectoexpression. (g) The defect of the ASH Ca²⁺ transients in the tph-1 mutants was rescued by application of 5 mM exogenous 5-HT. Summation of the kinematics of Cu²⁺ avoidance behaviours (h,i) and Cu²⁺ sensitivity (j, n≥8 assays) in the worms denoted. All data are expressed as means±s.e.m. The number on each bar indicates the number of independent tests for each genotype. One-way analysis of variance (ANOVA) test in a–c and f–i, and two-way ANOVA test in d and j. Corrected with Bonferroni t-test. Values that differ significantly are indicated (*P≤0.05, **P≤0.01 and ***P≤0.001 compared with the wild-type N2 control).