The ABCB1-gene product P-glycoprotein is an integral membrane protein that actively transports substrates out of the intracellular compartment. One of the major sites of its action is the blood-brain-barrier. It is highly expressed in brain capillary endothelial cells and involved in limiting the access of substrates such as antidepressants to the CNS. A single nucleotide polymorphism (SNP) of the ABCB1-gene was recently identified showing a different treatment response to antidepressant drugs depending on the genotype. Therefore, it is assumed that healthy subjects with different genotypes of that SNP will be associated with significantly different brain levels of the antidepressant escitalopram after 6 days of intake. For determining intracerebral escitalopram levels, a 19-F magnetic resonance spectroscopy will be used. Sleep recordings are a useful bio-marker for effects of antidepressants on the CNS. Selective 5-HT1-reuptake inhibitors (e.g. escitalopram) cause a suppression of REM sleep and a stronger fragmentation of sleep compared to untreated subjects. Higher plasma levels of antidepressants affected the sleep to a greater extent than lower levels. In line with this finding, we suppose that sleep EEG recordings of healthy subjects with different genotypes of the above mentioned SNP will be differently affected after taking 6 days escitalopram. In addition, there is good evidence that sleep is involved in various forms of memory processing. For example, it has been repeatedly shown that the performance in motor tasks (procedural learning) is correlated with the amount of stage 2 NonREM and REM sleep, respectively. Hence we hypothesize, that a drug-induced impairment of sleep (e. g. reduction of REM sleep) is associated with an impairment of procedural learning. In addition, effects of drug intake on the gene expression in lymphocytes and metabolic changes will be assessed. Functional magnetic resonance imaging will be applied to detect potential drug-induced changes of corticolimbic circuitries.