Reversible brain swelling in crucian carp (Carassius carassius) and goldfish (Carassius auratus) in response to high external ammonia and anoxia.
Autor: | Wilkie MP; Department of Biology and Institute for Water Science, Wilfrid Laurier University, Waterloo, Ontario N2L 3C5, Canada; Department of Biosciences, University of Oslo, Oslo, Norway. Electronic address: mwilkie@wlu.ca., Stecyk JA; Department of Biosciences, University of Oslo, Oslo, Norway; Department of Biological Sciences, University of Alaska Anchorage, Anchorage, USA., Couturier CS; Department of Biosciences, University of Oslo, Oslo, Norway., Sidhu S; Department of Biology and Institute for Water Science, Wilfrid Laurier University, Waterloo, Ontario N2L 3C5, Canada., Sandvik GK; Department of Biosciences, University of Oslo, Oslo, Norway., Nilsson GE; Department of Biosciences, University of Oslo, Oslo, Norway. |
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Jazyk: | angličtina |
Zdroj: | Comparative biochemistry and physiology. Part A, Molecular & integrative physiology [Comp Biochem Physiol A Mol Integr Physiol] 2015 Jun; Vol. 184, pp. 65-75. Date of Electronic Publication: 2015 Jan 09. |
DOI: | 10.1016/j.cbpa.2014.12.038 |
Abstrakt: | Increased internal ammonia (hyperammonemia) and ischemic/anoxic insults are known to result in a cascade of deleterious events that can culminate in potentially fatal brain swelling in mammals. It is less clear, however, if the brains of fishes respond to ammonia in a similar manner. The present study demonstrated that the crucian carp (Carassius carassius) was not only able to endure high environmental ammonia exposure (HEA; 2 to 22 mmol L(-1)) but that they experienced 30% increases in brain water content at the highest ammonia concentrations. This swelling was accompanied by 4-fold increases in plasma total ammonia (TAmm) concentration, but both plasma TAmm and brain water content were restored to pre-exposure levels following depuration in ammonia-free water. The closely related, ammonia-tolerant goldfish (Carassius auratus) responded similarly to HEA (up to 3.6 mmol L(-1)), which was accompanied by 4-fold increases in brain glutamine. Subsequent administration of the glutamine synthetase inhibitor, methionine sulfoximine (MSO), reduced brain glutamine accumulation by 80% during HEA. However, MSO failed to prevent ammonia-induced increases in brain water content suggesting that glutamine may not be directly involved in initiating ammonia-induced brain swelling in fishes. Although the mechanisms of brain swelling are likely different, exposure to anoxia for 96 h caused similar, but lesser (10%) increases in brain water content in crucian carp. We conclude that brain swelling in some fishes may be a common response to increased internal ammonia or lower oxygen but further research is needed to deduce the underlying mechanisms behind such responses. (Copyright © 2015 Elsevier Inc. All rights reserved.) |
Databáze: | MEDLINE |
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