Crucian carp, Carassius carassius, survives months without oxygen. During anoxia it needs to keep the energy expenditure low, particularly in brain, with its high rate of ATP use related to neuronal activity. This could be accomplished by reducing neuronal excitability through altered expression of genes involved in excitatory neurotransmission. Through cloning and the use of a recently developed real-time RT PCR approach, using an external RNA control for normalization, we investigated the effect of 1 and 7 days of anoxia (12ºC) on the expression of 29 genes, including 8 AMPA-receptor subunits, 6 NMDA-receptor subunits, 7 voltage-gated sodium and calcium channel, 4 glutamate transporters and 4 genes involved in NMDAR-mediated neuroplasticity. The subunits of the majority of the gene families had expression profiles similar to those observed in the normal mammalian brain, and showed remarkably stable expression during anoxia. This suggests that the genes may have similar functions in crucian carp and mammals, and that the excitatory abilities of the crucian carp brain are retained during anoxia. Although the data generally talk against profound neural depression ("channel arrest"), the NMDA receptor-subunit (NR) expression showed features that could mediate reduced neural excitability. Primarily, the NR2 subunit expression, which was dominated by NR2B and NR2D, resembled that seen in hypoxia-tolerant neonatal rats, and decreased anoxic expression of NR1, NR2C and NR3A indicated reduced numbers of functional NMDA receptors. We also report the full-length sequence of crucian carp NR1 mRNA, and a novel NR1 splice cassette introducing an N-glycosylation site into the extracellular S1S2 domain.