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Single episodes of ethanol intake generate only modest amounts of salsolinol, whereas chronic or binge-like exposure markedly increases salsolinol and N-methyl-salsolinol levels in dopaminergic regions such as the striatum and hypothalamus, as well as in biological fluids of alcohol-dependent subjects [31,32,33,34]

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[15] Bitter compounds activate T2Rs that release CCK during digestion