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Alcohol potentiates a pheromone signal in flies

  1. Annie Park  Is a corresponding author
  2. Tracy Tran
  3. Elizabeth A Scheuermann
  4. Dean P Smith
  5. Nigel S Atkinson  Is a corresponding author
  1. Department of Neuroscience and Waggoner Center for Alcohol and Addiction Research, The University of Texas at Austin, United States
  2. Department of Pharmacology and Neuroscience, University of Texas Southwestern Medical Center, United States
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Cite this article as: eLife 2020;9:e59853 doi: 10.7554/eLife.59853
5 figures and 2 additional files

Figures

Alcohol odor increases aggression in male flies.

(a) Traces of T1 sensilla recordings with a 300 ms exposure to air or vapor from 30% ethanol. (b) Hemolymph ethanol concentration (mg/mL) in flies in aggression arenas for 30 mins show no significant increases except with 20% ethanol (one-way ANOVA with Dunnett’s p<0.0001, n = 11–12). (c) Time spent fighting on ethanol-containing food (Control vs. 5% p=0.038 Kruskal-Wallis test with Dunn’s correction, n = 10–20). (d) Number of fights on ethanol-containing food (Control vs. 5% p=0.0012, statistical tests as in c). (e) Lunges on ethanol-containing food (Control vs. 5% p=0.0225, statistical tests as in c). (f) Latency to lunge (p=0.009, Log-rank Mantel-Cox with Bonferroni correction). (g) Cumulative latency of flies that lunged during the test (Control vs. 10% p=0.009, Log-rank Mantel-Cox with Bonferroni correction). (h) Locomotion as measured by line crossings during the test (Control vs. 20% p=0.0048, statistical tests as in 1 c). p<0.05 *; p<0.01 **; p<0.001 ***. Error bars denote SEM.

Alcohol odor potentiates the response to cVa.

(a) Experimental timeline and diagram of recording site on fly antenna. (b) Traces of cVa-sensing T1 neurons. The red bar denotes 300 ms cVa exposure. (c) Δ Spikes calculated as cVa-induced activity (1 s during and after cVa) – spontaneous activity (paired two-tailed t-test, p=0.002, n = 7,15,15). (d) Spontaneous activity before, during, and after ethanol exposure. Spontaneous activity calculated as the total number of spikes 10 s prior to cVa delivery/10 s (Pre- vs. Post-5% p=0.002, Pre- vs. Post-30% p<0.0001, During vs. Post-30% p=0.0152, Kruskal-Wallis test with Dunn’s correction). (e), (f), (g) Averaged spikes over time for air, 5% ethanol, and 30% ethanol, respectively. Red bar denotes 300 ms cVa exposure (h) Time constant (τ) of decay of the cVa-induced spikes (Mann-Whitney test, p=0.0043). p>0.05, n.s. (not significant); p<0.05 *; p<0.01 **; p<0.0001 ****. Error bars denote SEM.

Ethanol increases attraction to and potentiates the neuronal response of a food related odor.

(a) Paradigm used to evaluate farnesol responses pre- and post-ethanol treatment. Responses are shown in panels b-e. (b) Δ Spikes of farnesol-induced activity in ai2 sensilla, calculated as in 2b (paired two-tailed t-test, p=0.0059, n = 9–10). (c) Spontaneous activity before, during, and after ethanol exposure, calculated as in 2 c (Pre- vs. During Ethanol p=0.017, Pre- vs. Post-Ethanol p<0.0001, Kruskal-Wallis test with Dunn’s correction). (d, e) Traces from ai2 farnesol-sensing neurons. The red bar denotes a 300 ms farnesol exposure. (f) Graphic of the two-choice olfactory trap assay used to measure relative attraction to odors. (g) Preference Indices calculated as Number of flies in Choice 1-Number of flies in Choice 2/Total Number of flies. p>0.05, n.s. (not significant); p<0.05 *; p<0.01 **; p<0.0001 ****. Error bars denote SEM.

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