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. 2021 Jan 15;46(8):1432–1441. doi: 10.1038/s41386-020-00938-8

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© The Author(s), under exclusive licence to American College of Neuropsychopharmacology 2021

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Fig. 5 — The β2 subunit-containing nAChR antagonist DHβE (1 µM) depressed dopamine release in caudate and putamen of control and ethanol subjects (A). Dopamine release was compared across varying train stimulations (6 pulses at the indicated frequencies) before and after nAChR blockade with DHβE (1 µM) in caudate and putamen (B, C; values normalized to single-pulse values before DHβE application). Gene expression of cholinergic interneuron markers and several nAChR subunits was not changed following chronic alcohol consumption and abstinence (D, E). Error bars represent the SEM.