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First published online August 6, 2004
Journal of Experimental Biology 207, 3131-3139 (2004)
Published by The Company of Biologists 2004
doi: 10.1242/jeb.00979

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Hypoxic survival strategies in two fishes: extreme anoxia tolerance in the North European crucian carp and natural hypoxic preconditioning in a coral-reef shark

Göran E. Nilsson^1,* and Gillian M. C. Renshaw²

¹ Department of Molecular Biosciences, University of Oslo, PO Box 1041, NO-0316 Oslo, Norway
² School of Physiotherapy and Exercise Science, Griffith University, PMB 50 Gold Coast, Queensland 9726, Australia

View larger version (15K): [in a new window]   Fig. 1. Dying or surviving in hypoxia. The key to anoxic brain survival is to maintain brain ATP levels. In the hypoxia-intolerant animal (A), anaerobic ATP production (glycolysis) has a limited capacity to compensate for the decline in aerobic ATP production (oxidative phosphorylation) during hypoxia. Therefore, ATP production soon falls passively with falling oxygen levels. Because this fall is not matched by a corresponding reduction in ATP use, the result is that ATP levels plummet, leading to membrane depolarization and a cascade of degenerative processes. In the anoxic survivor (B), the fall in aerobic ATP production is initially compensated for by an elevated anaerobic ATP production and subsequently matched by an orchestrated suppression of ATP use called metabolic depression. Thereby, ATP levels are maintained.

View larger version (27K): [in a new window]   Fig. 2. (A–D) Effect of anoxia, exposure to a high K+ concentration and forced energy deficiency on the extracellular level of GABA and glutamate. In A,B, the filled circles represent the anoxia-exposed fish, while open circles represent control fish kept in normoxia during the whole experiment. Iodoacetate (IAA) was used to create energy deficiency during anoxia. The horizontal lines mark the periods of anoxia (N2 exposure), when a high-K+ Ringer was pumped through the microdialysis probe or when IAA was superfused onto the brain. Values are means ± S.E.M. from 6–8 fish. Redrawn from Hylland and Nilsson (1999).

View larger version (26K): [in a new window]   Fig. 3. Hypoxic-preconditioning on a coral reef platform like that of Heron Island. (A) At very low tides, the water on the platform gets cut off from the surrounding ocean, essentially forming a very large tide pool. If this happens at night, the respiration of the reef organisms will make the water hypoxic, particularly on calm nights with little wave action. (B) The tide chart shows a period where the tides become lower and lower over a few days. As a result, the time that the water on the reef platform is disconnected from the ocean will increase in length for each subsequent night, causing the nocturnal hypoxic episodes to become longer and longer and therefore increasingly severe. Such `natural preconditioning periods' occur once or twice per month.

View larger version (140K): [in a new window]   Fig. 4. Changes in glutamate (A) and GABA (B,C) immunoreactivity in the brainstem of the epaulette shark in response to hypoxic exposure. In A, the only statistically significant difference between the hypoxic (left) and control (right) animal occurred in the median longitudinal fasciculus (mlf), otherwise glutamate homeostasis was maintained, including the fasciculus of Steida (fSt). In B,C, a statistically significant increase in GABA immunoreactivity was observed in hypoxia (B) compared with normoxia (C) over the entire coronal section, and small GABAergic neurons were only evident in the mlf of animals exposed to hypoxia.

View larger version (90K): [in a new window]   Fig. 5. Nitric oxide synthase activity in the diencephalon of the epaulette shark in response to hypoxic exposure. The level of nitric oxide synthase (NOS) staining is uniformly low over the entire brain in control animals (A). After hypoxia (B), a striking NOS staining makes the vasculature clearly visible, showing that the endothelial cells have increased their NOS activity. See Renshaw and Dyson (1999) for experimental details.