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. 2022 Sep 13;11:e77411. doi: 10.7554/eLife.77411

Figure 3. Alterations in drinking microstructure represent significant decreases in alcohol intake and are predictive of AIC→DLS alcohol-induced synaptic plasticity changes.

Figure 3.

Photoexciting anterior insular cortex (AIC) inputs does not alter the (A) number of water licks (two-way mixed analysis of variance [ANOVA], Virus F(1,17) = 3.7529, p=0.0695; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals), (B) water lick durations (two-way mixed ANOVA, Virus F(1,17) = 2.2136, p=0.1551; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals), (C) water bouts (two-way mixed ANOVA, Virus F(1,17) = 3.0848, p=0.0971; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals), (D) latency to drink water (two-way mixed ANOVA, Virus F(1,17) = 2.7012, p=0.1186; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals), (E) mean inter-drink-interval for water drinking (two-way mixed ANOVA, Virus F(1,17) = 0.0272, p=0.8708; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals), (F) or the number water bouts in the first 30 min of the Drinking in the Dark (DID) session (two-way mixed ANOVA, Virus F(1,17) = 0.5716, p=0.4599; ChR2: 32 observations, n=8 animals, eGFP: 44 observations, n=11 animals). Photoexciting AIC inputs (G) decreases the number of alcohol licks (two-way mixed ANOVA, Virus F(1,14) = 11.0142, p=0.0051; Virus × Drinking Week F(3,42) = 5.8888, p=0.0019; Week 5 p=0.0307, Week 6 p=0.0137; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals), (H) decreases total alcohol lick duration (two-way mixed ANOVA, Virus F(1,14) = 6.9536, p=0.0195; Virus × Drinking Week F(3,42) = 3.8533, p=0.0160; Week 5 p=0.0458; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals), and (I) decreases the number of alcohol bouts (two-way mixed ANOVA, Virus F(1,14) = 11.2086, p=0.0048; Virus × Drinking Week F(3,42) = 9.4893, p=0.0001; Week 5 p=0.0135, Week 6 p=0.0051; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals). (J) Modulating AIC inputs does not impact the latency to drink alcohol (two-way mixed ANOVA, Virus F(1,14) = 0.0084, p=0.9281; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals) or (K) the mean inter-drink-interval for alcohol drinking (two-way mixed ANOVA, Virus F(1,14) = 0.4686, p=0.5047; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals), but (L) decreases front loading behaviors for alcohol drinking (two-way mixed ANOVA, Virus F(1,14) = 4.2003, p=0.0596; Virus × Drinking Week F(3,42) = 3.9078, p=0.0150; Week 6 p=0.0230; ChR2: 32 observations, n=8 animals, eGFP: 32 observations, n=8 animals). (M) Schematic for microstructure feature detection, dataset assembly, cross-validation, and network architecture. (N) Loss curve visualization for training and testing data. (O) Model accuracy for training and testing data. Error bars indicate ± SEM. All post hoc comparisons are Sidak corrected.

Figure 3—source code 1. Alterations in drinking microstructure represent significant decreases in alcohol intake and are predictive of AIC→DLS alcohol-induced synaptic plasticity changes.
Figure 3—source data 1. Alterations in drinking microstructure represent significant decreases in alcohol intake and are predictive of AIC→DLS alcohol-induced synaptic plasticity changes.