In patients with obsessive-compulsive disorder (OCD), structural and volumetric abnormalities have been identified by up-to-date neuroimaging techniques both in the prefrontal region and in the basal ganglia (striatum, thalamus, amygdala). The dysfunction of these regions also has been proved by neuroimaging techniques. These alterations can be described as dopaminergic hyperfunction in the prefrontal cortex and serotonergic hypofunction in the basal ganglia. The dysfunction of the so-called 'cortico-striato-thalamic' loops is strongly linked to the symptoms of OCD, where the dopamine is the most dominant neurotransmitter. The ascending serotonergic projections from the raphe nuclei restrain and control the function of these loops. Thus, when serotonergic hypofunction is present, the predominantly dopaminergic loops became overactive, which has been confirmed by neuroimaging techniques and by neurocognitive tests as well. The linkage of the two predominant neurotransmitter systems affected in OCD can be the reason for the fact that SSRIs have limited success in the treatment of OCD symptoms. In recent international, multicentric studies, the treatment of SSRI non-responder subgroup of OCD patients were supplemented by antipsychotics with dopaminergic activity. Many studies have confirmed the beneficial effect of these antidopaminergic substances on the hyperactive cortico-striato-thalamic loops in OCD. The investigation of these dysfunctional loops is also connected to the genetic background of OCD, because some of the candidate gene regions of OCD are coding proteins of the dopamine synthesis (for example: COMT). In this paper, we present a detailed overview of these relationships based on recent findings of OCD research.