Fig. 6: Chronic alcohol consumption increased dynorphin release probability in long-term abstinence. | Nature Communications

Fig. 6: Chronic alcohol consumption increased dynorphin release probability in long-term abstinence.

From: Synchrony between midbrain gene transcription and dopamine terminal regulation is modulated by chronic alcohol drinking

Fig. 6

A Representative traces indicating dopamine release in controls at 10 Hz and 60 Hz normalized to 1 pulse dopamine release before and after NorBNI. B Dopamine release in controls with and without NorBNI across stimulation frequencies. C There was no effect of a history of ethanol intake, but there was an effect of NorBNI, on the area under the curve (AUC) of dopamine release across frequencies (mixed model two-way ANOVA: ethanol history: F1, 14 = 0.03, p = 0.88; drug: F1, 14 = 6.152, p = 0.03). NorBNI had no effect on AUC of dopamine release in controls (Šídák’s test: baseline vs. NorBNI in controls: t14 = 0.66, p = 0.77). D Representative traces indicating dopamine release in controls at 10 Hz and 60 Hz normalized to 1 pulse dopamine release with and without NorBNI. E Dopamine release in drinkers with and without application of NorBNI across stimulation frequencies. AUC of dopamine release is visually represented by figure shading. F NorBNI administration increased the AUC of normalized dopamine release in drinkers suggesting significant dynorphin release at these stimulation intensities after chronic alcohol self-administration (mixed model two-way ANOVA: ethanol history: F1, 14 = 0.03, p = 0.88; drug: F1, 14 = 6.152, p = 0.03; Šídák’s test: baseline vs. NorBNI in drinkers: t14 = 2.85, p = 0.03). G, H Upstream expression of OPRK1 and PDYN were correlated within-subject with the proportion of change in AUC of dopamine release. The best-fit linear regression is shown for each group. Inset: Pearson’s r and p-values. G Expression of OPRK1 in the ventral tegmental area was positively correlated with the change in dopamine release with NorBNI administration in controls, not drinkers. H PDYN expression was also only correlated with the dynorphin release probability in controls, not drinkers. All statistical tests were two-tailed. Unless otherwise indicated, values indicate mean ± SEM. (*p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001, ****p ≤ 0.0001) (controls: n = 8; drinkers: n = 8).

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