Antipsychotic drugs are used in the treatment of psychotic disorders (delusions, hallucinations, thought disorders) in schizophrenia, and psychosis related to depression, bipolar disorder, and Alzheimer's disease. Two main types of these drugs are called typical and atypical antipsychotics. Unfortunately, some patients following antipsychotics treatment develop unwanted side effects, which often lead to treatment discontinuation and symptom relapse. The best-known side effects of typical antipsychotics are motor side effects such as dystonia, Parkinsonism, akathisia, and tardive dyskinesia, primarily due to the blockade of dopamine receptors in nigrostriatum and consequent excessive activity of acetylcholine system. However, given that there are strong neuroanatomical and functional interactions of serotonergic and dopaminergic systems, and that serotonergic system largely regulates and modulates the activity of dopaminergic system, and vice versa, it is possible that certain variations in the serotonergic genes may affect the development of motor side effects of typical antipsychotics, which act primarily via dopamine receptors. Therefore, in order to clarify the role of serotonin receptor genes in the development of the motor side effects, the aim of this diploma thesis was to investigate the possible association between two polymorphisms, in the gene coding for the serotonin 5-HT1A receptor, with the development of motor side effects following treatment with a typical antipsychotic haloperidol in patients with schizophrenia. Obtained results suggest no genotypic or haplotypic association of investigated polymorphisms in 5-HT1A gene with extrapyramidal side effects of haloperidol in schizophrenia patients.