Crucian carp (Carassius carassius L.), which are extremely anoxia-tolerant, were exposed to 17 days of anoxia at 8 degrees C. One group of fish was transferred to normoxic water for 1–8 h immediately after the anoxic period. All the eight amino acids measured in brain (including four putative neurotransmitters) were more or less strongly affected by anoxia. Gamma-aminobutyric acid (GABA) displayed a nearly fivefold increase during anoxia. It is hypothesized that the increased level of this inhibitory transmitter, maybe in combination with the decrease seen in excitatory amino acids (glutamate and aspartate), causes a lowered brain activity and, hence, is a key factor behind the decrease in physical activity and systemic energy metabolism seen in anoxic Carassius. The brain levels of serotonin, dopamine and norepinephrine were remarkably well preserved after anoxia (although their synthesis is oxygen-dependent), suggesting adaptive mechanisms. However, anoxia reduced the norepinephrine level in kidney (chromaffin tissue) by 92% and, in contrast to previous results on shorter anoxic periods (3–7 days), the peripheral catecholamine store showed little sign of recovery during the subsequent normoxia. Anoxia was found to deplete the liver glycogen store severely, and the few fish that died after 15–17 days of anoxia contained no detectable liver glycogen.

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