The crucian carp, Carassius carassius, survives days to months without oxygen, depending on temperature. In the anoxic crucian carp brain, increased GABAergic inhibition, mediated by increased extracellular levels of GABA, has been shown to suppress electric activity and ATP consumption. To investigate an involvement of gene expression in this response, we have utilized real-time RT PCR to investigated the effect of 1 and 7 days anoxia (8°C) on the expression of 22 genes, including 9 GABA_A receptor subunits (_1-6, ₂, and ₂), 3 GABA_B receptor subunits (GB1-1b and GB2), 3 enzymes involved in GABA metabolism (GAD65 and GAD67, GABAT), 4 GABA transporters (GAT1, 2a-b and 3), 2 GABA_A-receptor associated proteins (GABARAP 1 and 2) and the K⁺/Cl^- co-transporter KCC2. While the expression of GABA_A receptor subunits was dominated by ₄, ₆, and subunits, all of which are located to extrasynaptic sites in mammalian brains and respond to elevations in extracellular levels of GABA by showing tonic activity-patterns, the expression of GABA transporters was dominated by GAT2 (a and b) and GAT3, which also show extrasynaptic location in mammals. These expression patterns differ from those observed in mammals, and may be a prerequisite for GABAergic inhibition of anoxic metabolic rate in crucian carp. Furthermore, while the expression of the majority of the genes was largely unaltered by anoxia, the expression of GAT2 and GAT3 decreased to 20%. This suggests impairment of GABA transport, which could be a mechanism behind the accumulation of extracellular GABA and the increased GABAergic inhibition.