Chronic ethanol ingestion has been shown to induce significant changes in neurotransmitter systems, including serotonin (5HT). Increased ethanol consumption has been also related to a hypoactivity of brain serotonin system. By use of selective breeding we have developed a rat model with constitutionally different peripheral (platelet) serotonin level and activity of 5HT transporter: Wistar-Zagreb 5HT rat. These rat sublines demonstrated clear neurochemical and behavioral alterations indicating also differences in their brain 5HT neurotransmission. Animals from the low-5HT subline have higher alcohol preference in a free choice situation, as compared to the animals from the high-5HT subline. The aim of the present study was to evaluate the effect of ethanol on monoamine oxidase (MAO), mitochondrial enzyme that degrades 5HT, in order to test whether ethanol consumption influences its activity and if there are differences between mentioned rat sublines. Animals from high- and low-5HT rat sublines were exposed to forced ethanol consumption with gradually increasing ethanol concentration (3-12 %) in drinking water. At the end of experiment (day 33) animals were sacrificed and MAO activity was measured fluorimetrically in cortex, hippocampus and striatum. There were no differences in the velocities of either MAO-B or MAO-A isoezymes between ethanol- and water-drinking rats, irrespectively on analyzed brain region and rat subline. The effect of ethanol on kinetics of MAO was tested also in vitro. In striatum homogenates from both rat sublines ethanol significantly decreased MAO activity, due to substantial increase in the Km values (decrease in affinity). In conclusion, chronic (one month) ethanol drinking does not change brain MAO activity, similarly in hyper- or hyposerotonergic animals. In vitro ethanol significantly decreases MAO affinity toward substrate, probably acting on the enzyme structure. Again, serotonergic status of the animal has no influence.