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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Neurochem Int. 2016 Feb 3;98:122–128. doi: 10.1016/j.neuint.2016.01.008

Figure 4.

Figure 4

Enhancement of NIS-induced Swip by dop-2 mutation supports negative presynaptic regulation of DA signaling (A) Average thrashing plots show enhanced paralysis in dat-1(ok157); dop-2(vs105) double mutants compared to dat-1(ok157) mutants. DA neuron expression of dop-2 with the plasmid Pdat-1::dop-2 suppressed this enhancement. (B) dat-1(ok157); dop-2(vs105) double mutants have a significantly decreased average latency to paralysis compared to dat-1(ok157) mutants, and DA neuron expression of dop-2 rescues this effect up to dat-1(ok157) mutant levels. No significant difference was observed between dat-1(ok157) and dat-1(ok157); dop-2(vs105) (pdat-1::dop-2) transgenic animals. Data was analyzed using individual two-tailed Student’s t-tests. ****p<.0001. n ≥ 25 for each condition. (C) dop-2(vs105) animals have subtle, yet significant increase in Swip compared to N2 in water, and a greater enhancement in 1 μM and 10 μM NIS. cat-2(e1112) animals have significantly less paralysis than N2 in both doses of NIS. Data was analyzed by two-way ANOVA with Bonferroni posttests comparing genotypes at each dose of NIS. **p<.01, ****p<.0001. (D) Heat map analysis of animals in 5 μM NIS further demonstrates the increase in Swip in dop-2(vs105) mutants vs. N2. dop-2(vs105) showed a higher percentage of paralyzed animals (96.0% vs. 68.2% for N2), lower percentage of animals reverting to swimming (14.6% vs. 33.3% for N2) and significantly fewer average reversion events per paralyzed animal (2.14 ± 0.15 events vs. 4.40 ± 0.33 events for N2, p<.0001 two-tailed Student’s t-test). n ≥ 44 for each condition.