Reversible brain swelling in crucian carp (Carassius carassius) and goldfish (Carassius auratus) in response to high external ammonia and anoxia

• Published in: Comparative biochemistry and physiology. Part A, Molecular & integrative physiology Molecular & integrative physiology, 2015-06, Vol.184, p.65-75
• Main Authors: Wilkie, Michael P., Stecyk, Jonathan A.W., Couturier, Christine S., Sidhu, Sanya, Sandvik, Guro K., Nilsson, Göran E.
• Format: Article
• Language: English
• Subjects: Ammonia - administration & dosage; Ammonia toxicity; Animals; Astrocyte; Body Water; Brain; Brain Edema - etiology; Carps; Encephalopathy; Ethanol; Ethanol - metabolism; Glutamine; Glutamine synthetase; Goldfish; Hyperammonemia; Hypoxia; Methionine sulfoximine; Neurotoxicity
• ISSN: 1095-6433; 1531-4332
• DOI: 10.1016/j.cbpa.2014.12.038

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 22mmolL−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 3.6mmolL−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 96h 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.