Prenatal exposure to acute hypoxia can cause developmental disturbances and lifelong behavioral disorders the molecular background of which needs to be clarified to find effective therapy in the future. Although hypoxia is known to cause changes in the catecholamine system, the long-term consequences in specific brain regions have been poorly investigated. In our rat model of mild prenatal hypoxia, we have previously shown elevated brainstem dopamine levels and increased number of rearings, indicating impaired spatial mapping or sensoric processing. The aim of this study was to determine changes in gene expression of dopamine receptor 1 (Drd1) and 2 (Drd2) in the regions responsible for sensory processing (thalamus, somatosensory cortex) and spatial mapping (hippocampus). Hypoxia (8% O2, 92% N2) was induced in 16 experimental Wistar Han rats (8 females, 8 males) in a warm (≈ 27°C) chamber, for 2 hours on the first postnatal day (PND1). At the same time 15 control rats (8 females, 7 males) were kept under normoxic conditions (21% O₂, 78% N₂). On PND50 rats were sacrificed and thalamus, cortex and hippocampus were collected. Differential gene expression for Drd1 and Drd2 was determined using real-time PCR based on Taq-man probes, with Hprt1 and Actb as reference genes. In comparison to the control group, hypoxic rats displayed highly significant increase in the relative mRNA expression for Drd1 and Drd2 in thalamus, and for Drd1 in somatosensory cortex. Drd1 and Drd2 gene expression was not changed in the hippocampal tissue. Changes in the relative expression of Drd1 and Drd2 mRNA in thalamus and somatosensory cortex, indicated that altered exploratory behavior observed in this rat model may be caused by impaired sensory processing.